Psoriasis is a chronic, recurrent and systemic inflammatory skin disease which is mediated by immunoreaction. Its pathogenesis is multifactorial, and the exact driving factor remains unclear. Recent studies showed that gut microbiota, which maintain immune homeostasis of our bodies, is closely related with occurrence, development and prognosis of psoriasis. The intestinal microbial abundance and diversity in patients with psoriasis have changed significantly, including intestinal microbiota disorders and reduced production of short chain fatty acids (SCFAs), abnormalities in Firmicutes/Bacteroidetes (F/B), etc. Besides, the intestinal microbiota of psoriasis patients has also changed after treatment of systemic drugs, biologics and small molecule chemical drugs, suggesting that the intestinal microbiota may be a potential response-to-treatment biomarker for evaluating treatment effectiveness. Oral probiotics and prebiotics administration as well as fecal microbial transplantation were also reported to benefit well in psoriasis patients. Additionally, we also discussed the microbial changes from the skin and other organs, which regulated both the onset and treatment of psoriasis together with gut microbiota. Herein, we reviewed recent studies on the psoriasis-related microbiota in an attempt to confidently identify the "core" microbiota of psoriatic patients, understand how microbiota influence psoriasis through the gut-skin axis, and explore potential therapeutic strategies for psoriasis.

Psoriasis, with a global incidence rate of 2%-3%, afflicts patients with persistent erythema and scales and is often accompanied by comorbidities such as arthritis and depression, significantly impairing their quality of life. While emerging biologics and traditional medications as well as phototherapy have made certain progress in treating psoriasis, these therapies are hindered by significant drawbacks including high costs, suboptimal efficacy, and significant side effects. Photodynamic therapy (PDT) has great potential for psoriasis treatment, but its application is limited due to the weak penetration of short-wavelength light used for active photosensitizer (PS). Upconversion nanoparticles (UCNPs) offer a promising solution for traditional PDT as they could be excited by near-infrared (NIR) light to emit UV-visible light for reactive oxygen species generation, which effectively addresses penetration challenges. In this study, PS (ZnPc) was encapsulated on UCNPs coated with a porous silica shell (UCNPs-ZnPc). When topically applied to psoriatic mice skin, UCNPs-ZnPc was taken up by macrophages. Upon activation with 980 nm NIR light, psoriatic dermatitis was treated since the macrophage viability was reduced, and the overproliferation of psoriatic skin cells was suppressed. These results highlight the potential of UCNPs-mediated PDT as an innovative approach to managing psoriasis.

Psoriasis is defined as a persistent autoimmune disease characterized by the appearance of psoriatic lesions on the surface of the skin. Currently, various approaches including chemicals, corticosteroids, phototherapy, and biological agents are being proposed and implemented to improve psoriatic lesions by modulating immune system activity or metabolic processes, often with unintended consequences and side effects. Currently, mesenchymal stromal/stem cells (MSCs) have attracted considerable interest among researchers due to their ability to modulate immune responses and their ease of application, representing a promising strategy for alleviating clinical symptoms in the treatment of allergic reactions, autoimmune diseases, cancer, and more. This study will investigate how MSCs interact with immune system cells involved in psoriasis development, such as neutrophils, keratinocytes, dendritic cells (DC), and T cell subtypes, for potential therapeutic use in psoriasis management. In this case, several immunomodulatory mechanisms are involved, including expression of chemokines, pro-inflammatory cytokines, matrix metalloproteinase and other factors involved in cell proliferation and neutrophil extracellular trap (NET) formation are among the effects of MSCs on keratinocytes and neutrophils. keratinocytes and neutrophils as pro-inflammatory cells involved in psoriasis pathogenesis and pathogenesis and progression of psoriasis. On the other hand, MSCs interact with DCs and various subsets of T cells, including Th1, Th2, Th17 and Tregs, to generate tolerogenic DCs and increase the differentiation of Tregs and modulate the Th17/Treg towards a regulatory state through overexpression of anti-inflammatory and immunomodulatory and immunomodulatory cytokines, including IL-10 and transforming growth Factor beta (TGF-β). Finally, we will focus on the challenges and obstacles in psoriasis treatment using MSCs, including limitations in the case of using MSCs from different sources and side effects that may be encountered by whole cell therapy strategies, which are attracting attention towards the implication of cell-free regimens such as using MSC-derived secretome or extracellular vesicles and exosomes to provide similar therapeutic outcomes without presumed side effects.

Immune-mediated skin disorders arise from dysfunctional immune responses, instigating inflammatory dermatoses and a reduced quality of life. The complex pathogenesis likely involves genetic risks, environmental triggers and aberrant immune activation. An emerging body of evidence suggests that bile acid disturbances may critically promote immune pathology in certain skin conditions. Bile acids synthesised from cholesterol regulate nutrient metabolism and immune cell function via nuclear receptors and G protein-coupled receptors (GPCRs). Altered bile acid profiles and receptor expression have been identified in psoriasis, atopic dermatitis (AD) and autoimmune blistering diseases. Disruptions in bile acid signalling affect the inflammatory and metabolic pathways linked to these disorders. Targeting components of the bile acid axis represents a promising therapeutic strategy. This review elucidates the intricate links between bile acid homeostasis and immune dysfunction in inflammatory skin diseases, synthesising evidence that targeting bile acid pathways may unlock innovative therapeutic avenues. This study compiles clinical and experimental data revealing disrupted bile acid signalling and composition in various immune-mediated dermatoses, highlighting the emerging significance of bile acids in cutaneous immune regulation.

Psoriasis is characterized by abnormal differentiation and hyperproliferation of epidermal keratinocytes. This condition presents significant challenges for effective drug delivery. In addition to overcoming the thickness of the skin, topical treatments must navigate the complex hydrophobic and hydrophilic properties of the skin barrier. Recent advancements in nanocarrier technologies, including energy-driven methods and microneedles that penetrate the stratum corneum, present promising strategies for enhancing drug permeation through tailored physicochemical properties. A literature search was performed using the databases of Google Scholar, PubMed, and ScienceDirect.

This review highlights recent studies on novel topical delivery methods for psoriasis treatment, addressing current therapeutic options and their limitations. We provide a comprehensive overview of chemical nanoformulations and explore physical strategies to improve delivery rates. Furthermore, we discuss the advantages of various formulations that can carry different types of payloads, offering patients diverse strategies for symptom management. The review covers conventional treatments, emphasizing advancements in nanoparticle design and novel macromolecular drugs. This includes Ribonucleic acid (RNA)-based therapies that protect macromolecular drugs from rapid clearance in the body.

We argue that intelligent design approaches can enhance efficacy across delivery applications while allowing for precision in treatment strategies, ultimately improving patient outcomes.

Psoriasis is a chronic and recurrent inflammatory disease driven not only by intrinsic factors such as immune system dysregulation but also by external factors, including bacterial infections. In contrast to the control of a single pathogenic pathway, combination therapies addressing both the immune and infectious components of psoriasis pathogenesis may offer a more effective strategy for controlling its progression. In this study, we developed a sprayable hydrogel incorporating tea polyphenol-loaded lauric acid liposomes (TP@LA-Lipo gel) to investigate its anti-inflammatory and antibacterial role in psoriasis. Our results demonstrated that TP@LA-Lipo modulated macrophage activity, reduced the expression of iNOS and TNF-α, and remodeled the immune microenvironment. Meanwhile, TP@LA-Lipo effectively eliminated Staphylococcus aureus and Escherichia coli through membrane disruption, mitigating the provoked inflammatory response. More importantly, TP@LA-Lipo gel, when sprayed onto the psoriasis lesions, provided sustained drug release over three days, enabling deeper penetration through the thickened stratum corneum to reach the inflamed layers beneath. Furthermore, in an imiquimod-induced psoriasis mouse model, TP@LA-Lipo gel effectively restored the damaged skin, alleviated histopathological changes, and reduced the systemic immune response. In summary, these findings indicate that TP@LA-Lipo gel offers a comprehensive strategy for effective disease management and improving the quality of life for psoriasis patients.

Industrialization and modernization have changed the environment. A group of emerging contaminants (ECs) has been defined recently. Psoriasis, whose incidence has increased in recent years, is a relapsing immune-mediated disease carrying a heavy disease burden. The erythematous scaly plaque is a typical symptom and occurs on several parts of the body. In addition, psoriasis has many comorbidities, such as psoriatic arthritis, diabetes, and depression, damaging the quality of life of patients. IL-17, IL-12, IL-23, and TNF-alpha are important related cytokines. ECs can influence psoriasis through the immune system and inflammatory responses. Specific mechanisms include increasing pro-inflammatory cytokines such as TNF-α and IL-17, and activating immune cells such as macrophages. And for psoriasis patients, it is suggested to reduce the exposure of most ECs. However, the complex mechanisms involved have not been discussed together and concluded. In this review, we summarize the relationship between ECs and psoriasis, focusing on the immune system, especially the immune cells and cytokines. These results can help guide clinical treatment and long-term management of psoriasis.

Immune-mediated inflammatory diseases (IMIDs) are chronic inflammatory diseases caused by immune system dysregulation, affecting multiple systems and organs. Children and adolescents aged 10-24 are among the high-risk groups, and the global burden is substantial.

Using the latest data from global burden of disease (GBD) 2021, we employed Joinpoint regression analysis, Socio-Demographic Index (SDI) correlation analysis, and cross-national equity analysis to elucidate the spatiotemporal differences in the burden of IMIDs among 10-24-year-olds from 1990 to 2021.

The burden of IMIDs in adolescents aged 10-24, ranked by severity, includes asthma, atopic dermatitis (AD), psoriasis, diabetes, rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and multiple sclerosis (MS). Among these, asthma, AD, psoriasis, RA, and MS are more prevalent in females. Compared to 1990, the incidence rates of asthma and AD decreased in 2021, while the rates of psoriasis, diabetes, and RA increased. IMIDs are more common in Western Europe and North America, with rising incidence rates in South America and Asia. Concentration indices and slope indices indicate that these diseases are primarily concentrated in high SDI regions, although the differences in incidence rates between countries are decreasing.

While focusing on high-incidence regions, we must also pay attention to the incidence of IMIDs in emerging regions such as Asia and South America. Only in this way can we effectively reduce the heavy burden that IMIDs place on younger people globally.

Plaque psoriasis (PP) is a chronic immune-mediated skin disorder with a genetic basis, characterized by abnormal T-cell responses. This study investigated the role of FOXP3 gene variants rs2280883 and rs3761548 in T-cell regulation through their effects on IL-10 and TGF-β1 cytokine levels and their association with PP risk. A case-control study was conducted, including 101 individuals with PP and 106 healthy controls from the Mexican population. Genotyping of FOXP3 variants was performed using PCR-RFLP, and cytokine levels were measured with ELISA kits. Significant differences in allele and genotype frequencies of the rs2280883 variant were observed between PP patients and controls, suggesting an association with an increased risk of PP. IL-10 levels were found to be elevated in PP patients, regardless of FOXP3 gene variants, indicating that cytokine dysregulation in PP may involve alternative pathways independent of FOXP3-mediated regulatory T-cell (Treg) function. No significant differences were detected in TGF-β1 levels or rs3761548 genotype frequencies across the study groups. In conclusion, the rs2280883 variant in the FOXP3 gene is significantly associated with a higher risk of developing PP in the Mexican population, while dysregulated IL-10 levels suggest a complex cytokine interaction beyond Treg activity.

Air pollution and genetic risk have been found to contribute to the onset and development of psoriasis. However, the extent to which genetic susceptibility modifies the effects of air pollutants on the risk of incident psoriasis remains unknown.

To assess the association between joint exposure to multiple air pollutants and the risk of psoriasis, and its modification, according to genetic susceptibility.

This prospective study included 451 064 participants from the UK Biobank who had complete air pollution data and were free of psoriasis at baseline. All participants were enrolled from 2006 to 2010 and followed up to 2022. An air pollution score (APS) was calculated to assess joint exposure to multiple air pollutants, including fine particulate matter (PM) with diameters ≤ 2.5 μm (PM2.5), between 2.5 and 10 μm (PM2.5-10) and ≤ 10 μm (PM10), as well as nitrogen dioxide (NO2) and nitrogen oxides (NOx). To evaluate the genetic risk, a polygenic risk score (PRS) for psoriasis was constructed. Cox proportional hazard models were used to assess the association of air pollution and genetic susceptibility with the risk of psoriasis. Stratified analyses were conducted based on the individual characteristics.

During a median follow-up of 13.79 years (range 0.00-16.81), 4414 cases of psoriasis were recorded. The hazard ratios (HRs) for psoriasis were 1.036 [95% confidence interval (CI) 0.936-1.147], 1.091 (95% CI 0.987-1.206), 1.159 (95% CI 1.048-1.283) and 1.163 (95% CI 1.052-1.286) in the higher APS quintile groups (Q2, Q3, Q4 and Q5, respectively) vs. the lowest APS quintile (Q1; P-value for trend < 0.05). When considering genetic susceptibility, participants with a high PRS and a high APS had the greatest risk of incident psoriasis (HR 1.962, 95% CI 1.630-2.362) vs. those with a low PRS and low APS. The HRs for PM2.5-10, NOx, PM2.5 absorbance, PM2.5, NO2 and PM10 in the group with the highest exposure level and genetic risk were 1.831 (95% CI 1.537-2.181), 1.722 (95% CI 1.431-2.073), 1.698 (95% CI 1.416-2.037), 1.619 (95% CI 1.353-1.938), 1.504 (95% CI 1.252-1.806) and 1.425 (95% CI 1.192-1.704), respectively.

Long-term exposure to various air pollutants is positively associated with an increased risk of incident psoriasis, particularly in individuals with a high genetic risk of the disease. More comprehensive measures are needed to reduce the air pollution levels for better prevention of psoriasis.

Psoriasis, a widespread and chronic inflammatory skin disorder, is marked by its persistence and the lack of a definitive cure. The pathogenesis of psoriasis is increasingly understood, with ongoing research highlighting the intricate interplay of genetic, immunological, and environmental factors. Recent advancements have illuminated the pivotal role of microRNAs in orchestrating complex processes in psoriasis and other hyperproliferative skin diseases. This narrative review highlights the emerging significance of miRNAs as key regulators in psoriasis pathogenesis and examines their potential as therapeutic targets. We discuss current treatment approaches and the promising future of miRNAs as next-generation therapeutic agents for this condition.

Psoriasis is a long-lasting inflammatory skin condition characterized by excessive keratinocyte growth. Recent studies have confirmed abnormal regulation of microRNAs (miRNAs/miRs) in individuals with psoriasis. This study aimed to investigate the function and specific mechanism of action of miR-128a-3p in interleukin-22 (IL-22)-stimulated HaCaT cells. The expression level of miR-128-3p and sirtuin 1 (SIRT1)/hypoxia inducible factor (HIF-1α) was detected using qRT-PCR on patients with psoriasis and IL-22-treated HaCaT cell model. Western blotting was used to detect apoptosis-associated proteins and SIRT1/HIFα pathway protein expression levels. The cell viability was determined using the CCK-8 method. Flow cytometry was performed to detect apoptosis following IL-22 stimulation or transfection. Enzyme-linked immunosorbent assay (ELISA) was used to detect cellular inflammatory factor secretion. The relationship between miR-128-3p and SIRT1 was predicted using the Starbase database and verified using a dual-luciferase reporter gene assay. In patients with psoriasis and IL-22-stimulated HaCaT cells, miR-128-3p and HIF-1α expression levels were elevated and SIRT1 expression was decreased. miR-128-3p directly targeted SIRT1. IL-22 stimulation significantly elevated cell viability, inhibited apoptosis levels and cleaved-caspase3 protein expression, and promoted an inflammatory response in HaCaT cells, which was further promoted by the miR-128-3p mimic. The miR-128-3p inhibitor reduced cell viability, promoted cell apoptosis and cleaved-caspase3 protein expression, and inhibited the inflammatory response in IL-22-induced HaCaT cells; these effects were at least partly reversed by SIRT1-siRNA. miR-128-3p expression is elevated in psoriasis and promotes psoriasis progression by inhibiting SIRT1 expression.

Biological therapies, including TNF-alpha, IL12/23, IL17 and IL23 antagonists, adequately control a very high number of patients with moderate-to-severe psoriasis with an excellent long-term safety profile. However, on occasion, patients on biological therapy with stabilized disease or complete remission report episodes of sudden breakthrough psoriasis.

To study prospectively in a monocentric tertiary setting, the clinical characteristics of patients presenting a sudden breakthrough psoriasis although completely stabilized (PASI 90-100) under biological therapy.

Psoriasis patients treated by biological therapies achieving PASI 90-100 and with stabilized disease for at least 6 months were invited to enter the follow-up study for 5 years. The clinical features of patients presenting a breakthrough psoriasis were described as well as the rescue therapies and outcomes.

From the total cohort of 1121 patients with psoriasis receiving biologicals, 985 patients responded to the inclusion criteria. After 5 years, 10/882 cases (1,13%) of breakthrough psoriasis were identified. Two cases were induced by the Köbner phenomenon and 8 cases by severe psychological stress. Rescue therapies included topical very potent corticosteroids or additional injections of the biological. Two patients recovered spontaneously when the stressful event was resolved. In none of the cases, there was a consistency between the breakthrough event and the next scheduled injection, nor the duration of the exposure to the treatment. No biological class or agent could be systematically incriminated.

Breakthrough psoriasis is an exceptional event among patients with stabilized psoriasis using biologicals, either triggered by the Köbner phenomenon or by severe psychological stress. The pathogenesis of the breakthrough events could be linked to stress- or Köbner-related immunomodulation, permitting breakthrough psoriasis lesions to appear.

In recent years, cancer immunotherapy has introduced novel treatments, such as monoclonal antibodies, which have facilitated targeted therapies against tumor cells. Programmed death-1 (PD-1) is an immune checkpoint expressed in T cells that regulates the immune system's activity to prevent over-activation and tissue damage caused by inflammation. However, PD-1 is also expressed in tumor cells and functions as an immune evasion mechanism, making it a therapeutic target to enhance the immune response and eliminate tumor cells. Consequently, immune checkpoint inhibitors (ICIs) have emerged as an option for certain tumor types. Nevertheless, blocking immune checkpoints can lead to immune-related adverse events (irAEs), such as psoriasis and cytokine release syndrome (CRS), as exemplified in the clinical case presented by Zhou et al involving a patient with advanced gastric cancer who received sintilimab, a monoclonal antibody targeting PD-1. Subsequently, the patient experienced exacerbation of psoriasis and CRS. The objective of this editorial article is to elucidate potential immunologic mechanisms that may contribute to the development of CRS and psoriasis in patients receiving ICIs. It is crucial to acknowledge that while ICIs offer superior safety and efficacy compared to conventional therapies, they can also manifest irAEs affecting the skin, gastrointestinal tract, or respiratory system. In severe cases, these irAEs can lead to life-threatening complications such as circulatory shock or multiorgan failure. Consequently, it is recommended that patients receiving ICIs undergo regular monitoring to identify and manage these adverse events effectively.

Psoriasis is a chronic skin condition characterized by immune-mediated inflammation. Recent research suggests a possible interaction between Helicobacter pylori infection and the immunopathogenesis of psoriasis. However, over the past 5 years, no significant new evidence has clarified the relationship between H. pylori and skin diseases. This study aimed to determine the relationship between H. pylori infection and psoriasis through a systematic review and meta-analysis.

We searched for articles published in databases including PubMed, Embase, the China National Knowledge Infrastructure, and Web of Science up to January 1, 2024. Statistical analyses were conducted using Review Manager 5.3 and Stata 12.0 software.

Our search yielded 271 papers. After rigorous screening by multiple reviewers, 15 studies involving 2,427 individuals were included. The odds ratio for H. pylori infection was significantly higher in the psoriasis group than in the control group (odds ratio = 1.94, 95% confidence interval: 1.40-2.68, p < 0.0001). Subgroup analysis revealed no significant differences in H. pylori infection rates between Asia and Europe. The type of study also did not significantly affect infection rates. The enzyme-linked immunosorbent assay detected H. pylori infection at a significantly higher rate than the breath test. Furthermore, the prevalence of H. pylori infection differed significantly between patients with moderate-to-severe psoriasis and those with mild psoriasis.

Our findings suggest a relationship between psoriasis and H. pylori infection, with variations observed based on geography, testing methods, and disease severity. These findings hold significant potential for guiding clinical practice.

http://www.crd.york.ac.uk/, identifier CRD42022359427.

Although the HaCaT keratinocyte model has been used in previous research to study the effects of antipsoriatic agents, there is still a lack of comprehensive understanding of the mechanism of imiquimod (IMQ)-induced proliferation and signal transduction in psoriasis-like keratinocytes.

This study aimed to investigate the molecular mechanisms and pathways associated with psoriasis-like inflammation caused by IMQ in human keratinocytes.

HaCaT cells were exposed to different concentrations of IMQ to induce inflammation similar to that observed in psoriasis. Cell viability was evaluated using the MTT assay and cell morphology was examined using phase-contrast microscopy. Gene expression profiles were analyzed through whole transcriptome sequencing, followed by bio-informatics network analysis using IPA software. The GSEA was conducted with the aim of identifying enriched pathways. The expression of key cytokines IL-6 and TNF-α was confirmed by QPCR. Artificial intelligence/machine learning (AI/ML) algorithms were used to predict potential diseases and phenotypes associated with the observed gene profiles.

IMQ treatment demonstrated a substantial positive impact on cell survival without any detectable alterations in the morphology of HaCaT cells. A comprehensive analysis of the entire set of transcribed genes identified 513 genes that exhibited differential expression. Bioinformatics analysis revealed key pathways associated with immune response, cellular proliferation, and cytokine signaling. GSEA identified significant enrichment in the IFN-γ response and JAK-STAT signaling pathways. QPCR analysis confirmed the increased mRNA expression levels of IL-6 and TNF-α in cells treated with IMQ. AI/ML algorithms have identified potential correlations with diseases, such as multiple sclerosis, lympho-proliferative malignancy, and autoimmune disorders.

Our results highlight the importance of specific genes and pathways, particularly those associated with IFN-γ pathway and IL-6/JAK-STAT signaling. AI/ML predictions indicate potential associations with various diseases and provide valuable insights for the development of novel therapeutic approaches for psoriasis and related disorders.

Psoriasis is a chronic, immunologically mediated disease of multifactorial origin, with genes playing a key role and environmental factors, such as infections, often triggering its onset or exacerbation. While acute streptococcal infections are commonly linked to guttate psoriasis, viral and fungal infections have also been associated with psoriasis flares. We report a case of severe psoriasis exacerbation during viral parotitis caused by paramyxovirus in a 49-year-old male patient with a long-standing psoriasis diagnosis. Following successful treatment with secukinumab, the patient experienced a flare-up coinciding with symptoms of mumps infection. Serological tests confirmed the presence of mumps virus RNA. Secukinumab was discontinued, and treatment with risankizumab resulted in rapid remission of psoriasis. While paramyxovirus infections are not typically associated with psoriasis flares, emerging evidence suggests that dysregulated antiviral immune responses may induce IL-23 production, possibly contributing to inflammation in psoriasis. This case highlights the need for further research on the role of antiviral immune responses in psoriasis exacerbations and the potential therapeutic implications of targeting the IL-23 pathway.

Rupioid psoriasis is a rare subtype of psoriasis characterized by distinctive lesions resembling oyster shells, known as rupioid lesions. This subtype is particularly uncommon in the pediatric population and is often associated with poor treatment compliance. Ustekinumab, an IgG monoclonal antibody, targets IL-12 and IL-23, reducing the release of proinflammatory cytokines TNFα, IL-2, and IL-17α, which play vital roles in psoriasis pathophysiology. Approved for pediatric patients aged six years and older, ustekinumab provides a therapeutic option for moderate to severe psoriasis. We present the case of a 10-year-old girl diagnosed with psoriasis vulgaris at age two. She presented with rupioid lesions following a urinary tract infection that had been treated with oral cefixime (200 mg). After conducting appropriate tests, ustekinumab (45 mg subcutaneously) was administered, leading to significant improvements in the thickness of the lesions and overall appearance. This case demonstrates ustekinumab's efficacy in treating this challenging form of psoriasis.

Artemisinin and its derivatives are widely recognized as first-line treatments for malaria worldwide. Recent studies have demonstrated that artemisinin-based antimalarial drugs, such as artesunate, dihydroartemisinin, and artemether, not only possess excellent antimalarial properties but also exhibit antitumor, antifungal, and immunomodulatory effects. Researchers globally have synthesized artemisinin derivatives like SM735, SM905, and SM934, which offer advantages such as low toxicity, high bioavailability, and potential immunosuppressive properties. These compounds induce immunosuppression by inhibiting the activation of pathogenic T cells, suppressing B cell activation and antibody production, and enhancing the differentiation of regulatory T cells. This review summarized the mechanisms by which artemisinin and its analogs modulate excessive inflammation and immune responses in rheumatic and skeletal diseases, autoimmune inflammatory diseases, and autoimmune disorders, through pathways including TNF, Toll-like receptors, IL-6, RANKL, MAPK, PI3K/AKT/mTOR, JAK/STAT, and NRF2/GPX4. Notably, in the context of the NF-κB pathway, artemisinin not only inhibits NF-κB expression by disrupting upstream cascades and/or directly binding to NF-κB but also downregulates multiple downstream genes controlled by NF-κB, including inflammatory chemokines and their receptors. These downstream targets regulate various immune cell functions, apoptosis, proliferation, signal transduction, and antioxidant responses, ultimately intervening in systemic autoimmune diseases and autoimmune responses in organs such as the kidneys, nervous system, skin, liver, and biliary system by modulating immune dysregulation and inflammatory responses. Ongoing multicenter randomized clinical trials are investigating the effects of these compounds on rheumatic, inflammatory, and autoimmune diseases, with the aim of translating promising preclinical data into clinical applications.

Mesenchymal stem cells (MSCs) are multilineage differentiating stromal cells with extensive immunomodulatory and anti-inflammatory properties. MSC-based therapy is widely used in the treatment of various pathologies, including bone and cartilage diseases, cardiac ischemia, diabetes, and neurological disorders. Along with MSCs, it is promising to study the therapeutic properties of exosomes derived from MSCs (MSC-Exo). A number of studies report that the therapeutic properties of MSC-Exo are superior to those of MSCs. In particular, MSC-Exo are used for tissue regeneration in various diseases, such as healing of skin wounds, cancer, coronary heart disease, lung injury, liver fibrosis, and neurological, autoimmune, and inflammatory diseases. In this regard, it is not surprising that the scientific community is interested in studying the therapeutic properties of MSCs and MSC-Exo in the treatment of psoriasis. This review summarizes the recent advancements from preclinical and clinical studies of MSCs and MSC-Exo in the treatment of psoriasis, and it also discusses their mechanisms of therapeutic action involved in the treatment of this disease.

Psoriasis is a chronic inflammatory skin disease characterized primarily by erythema and scales, having a wide-ranging impact globally. Previous studies have suggested that dietary consumption habits may influence psoriasis. The objective of this study was to determine the causal relationship between dietary consumption habits and psoriasis using the Mendelian Randomization (MR) approach.

SNP data for 29 dietary consumption habits and psoriasis were obtained from the GWAS catalog database and the FinnGen database, respectively. The Mendelian Randomization analysis was performed using R software, with the 29 dietary consumption habits as the exposure factors and psoriasis as the outcome. Three MR analysis methods-Inverse Variance Weighted (IVW), Weighted Median Estimator (WME), and MR-Egger regression-were employed to study the causal relationship between dietary consumption habits and psoriasis.

The IVW analysis indicated an OR (95%CI) of 0.065 (0.008-0.555), p = 0.012, demonstrating a negative correlation between the consumption of dried fruit and psoriasis.

Among the 29 dietary consumption habits analyzed, the intake of dried fruits is a protective factor against psoriasis. Therefore, it is clinically advisable to appropriately increase the intake of dried fruits among patients with psoriasis, serving as a nutritional therapy method in conjunction with pharmacological treatment.

The microbiome connects the gut health to the rest of the body's organs, including the skin. The pathophysiology of intestinal dysbiosis leads to the expression "leaky gut." Ongoing speculations are aimed at restoring the gut microbiota via modulating lifestyle habits to prevent and potentially reverse autoimmunity. This review finds the connections between gut dysbiosis and skin conditions. It also collects evidence of some lifestyle pillars that influence the gut microbiome including dietary intakes, exercise, sleep, stress, and toxin exposures. It addresses why maintaining a healthy intestinal microbiome is important for the health of all organs in the human host. More people are affected by gut dysbiosis resulting in pro-inflammatory effects on different organs, like the cutaneous tissue, one of the largest epithelial surfaces. It is essential to take care of the gut health because this is where most of the immune system resides. The connection between the intestinal tract with its microbiota and the cutaneous system with its microbiota seems to be mediated by the immune system of the human host. Therefore, this review enhances the understanding of the research on the gut microbiome, its relationship to skin health, and the interplay between the gut and various autoimmune cutaneous conditions.

Regulatory T cells (Tregs), a subset of CD4+T cells marked by the expression of the transcription factor forkhead box protein 3 (Foxp3), are pivotal in maintaining immune equilibrium and preventing autoimmunity. In our review, we addressed the functional distinctions between Foxp3+Tregs and other T cells, highlighting their roles in autoimmune diseases and cancer. We uncovered the dual nature of Tregs: they prevented autoimmune diseases by maintaining self-tolerance while contributing to tumor evasion by suppressing anti-tumor immunity. This study underscored the potential for targeted therapeutic strategies, such as enhancing Treg activity to restore balance in autoimmune diseases or depleting Foxp3+Tregs to augment anti-tumor immune responses in cancer. These insights laid the groundwork for future research and clinical applications, emphasizing the critical role of Foxp3+Tregs in immune regulation and the advancement of next-generation immunotherapies.

Psoriatic arthritis (PsA) is a chronic immunoinflammatory disease of the enthesis and adjacent synovium, skin, and nail, which early diagnosis may be crucial for starting a prompt therapeutic intervention. Theoretically, early treatment offers the advantage of acting on the reduction of the articular damage progression since initial phases of the disease.

This review explores the challenges of clinical-diagnostic aspects and the underlying pathophysiology of early PsA phases, as well as the evidence evaluating the impact of early intervention on disease outcomes.

Main instruments for early PsA diagnosis include recognizing synovial-entheseal inflammatory signs at onset, improving screening PsA high-risk subjects, and increasing disease knowledge of physicians and patients with psoriasis or familial history. PsA continues to significantly impact on the Quality of Life of patients affected by the disease, making necessary to deeply study clinical manifestations, risk factors, and underlying immunoinflammatory mechanisms, as well as to identify biomarkers for early identification. Additionally, it remains a need to increase more evidence on understanding how early treatment of PsA and of psoriasis might influence the course of the disease.

Psoriasis is one of the most common autoimmune skin diseases. Increasing evidence shows that alterations in the diversity and function of microbiota can participate in the pathogenesis of psoriasis through various pathways and mechanisms.

To review the connection between microbial changes and psoriasis, how microbial-targeted therapy can be used to treat psoriasis, as well as the potential of prebiotics, probiotics, synbiotics, fecal microbiota transplantation, diet, and Traditional Chinese Medicine as supplementary and adjunctive therapies.

Literature related to the relationship between psoriasis and gut microbiota was searched in PubMed and CNKI.

Adjunct therapies such as dietary interventions, traditional Chinese medicine, and probiotics can enhance gut microbiota abundance and diversity in patients with psoriasis. These therapies stimulate immune mediators including IL-23, IL-17, IL-22, and modulate gamma interferon (IFN-γ) along with the NF-kB pathway, thereby suppressing the release of pro-inflammatory cytokines and ameliorating systemic inflammatory conditions.

This article discusses the direction of future research and clinical treatment of psoriasis from the perspective of intestinal microbiota and the mechanism of traditional Chinese medicine, so as to provide clinicians with more comprehensive diagnosis and treatment options and bring greater hope to patients with psoriasis.

Psoriasis is a chronic inflammatory disease that affects around 2-3% of the world's population. The treatment for this autoimmune disease still remains centered around conventional methods using synthetic substances, even though more recent advancements focus on biological therapies. Given the numerous side effects of such treatments, current research involves plant extracts and constituents that could prove useful in treating psoriasis. The aim of this narrative review is to highlight the most known representatives belonging to classes of natural compounds such as polyphenols (e.g., astilbin, curcumin, hesperidin, luteolin, proanthocyanidins, and resveratrol), alkaloids (e.g., berberine, capsaicin, and colchicine), coumarins (psoralen and 8-methoxypsoralen), and terpenoids (e.g., celastrol, centelloids, and ursolic acid), along with plants used in traditional medicine that could present therapeutic potential in psoriasis. The paper also provides an overview of these compounds' mechanisms of action and current inclusion in clinical studies, as well as an investigation into their potential incorporation in various nanotechnological systems, such as lipid-based nanocarriers or polymeric nanomaterials, that may optimize their efficacy during treatment.

Psoriasis is a chronic inflammatory skin disease, the etiology of which has not been fully elucidated, in which CD8+ T cells play an important role in the pathogenesis of psoriasis. However, there is a lack of in-depth studies on the molecular characterization of different CD8+ T cell subtypes and their role in the pathogenesis of psoriasis. This study aims to further expound the pathogenesy of psoriasis at the single-cell level and to explore new ideas for clinical diagnosis and new therapeutic targets. Our study identified a unique subpopulation of CD8+ T cells highly infiltrated in psoriasis lesions. Subsequently, we analyzed the hub genes of the psoriasis-specific CD8+ T cell subpopulation using hdWGCNA and constructed a machine-learning prediction model, which demonstrated good efficacy. The model interpretation showed the influence of each independent variable in the model decision. Finally, we deployed the machine learning model to an online website to facilitate its clinical transformation.

Psoriasis is a chronic inflammatory cutaneous disease with multifactorial pathogenesis involving both genetic and environmental factors as well as the innate and acquired immune response. Several triggering factors may exacerbate or worsen the disease. In this context, we performed a review manuscript with the aim of investigating current literature on psoriasis risk factors, also showing possible mechanisms by which they act on psoriasis. Globally, risk factors can be divided in classic risk factors (eg, mechanical stress, infections and dysbiosis of the skin, common drugs, environment and pollution, lifestyle, psychological stress, hormonal and metabolic alterations) which have long been known to be responsible for worsening and/or reoccurrence of psoriatic manifestations, and emerging risk factors (eg, biological drugs, immunotherapy for oncologic disease, Covid-19, and vaccines) defined as those newly identified risk factors. Accurate patient information and monitoring of risk factors as well as planned follow-ups may help to prevent and treat the worsening of psoriasis and consequently improve the quality of life of psoriatic patients.

Skin macrophages are critical to maintain and restore skin homeostasis. They serve as major producers of cytokines and chemokines in the skin, participating in diverse biological processes such as wound healing and psoriasis. The heterogeneity and functional diversity of macrophage subpopulations endow them with multifaceted roles in psoriasis development. A distinct subpopulation of skin macrophages, characterized by high expression of CD169, has been reported to exist in both mouse and human skin. However, its role in psoriasis remains unknown. Here, we report that CD169+ macrophages exhibit increased abundance in imiquimod (IMQ) induced psoriasis-like skin lesions. Specific depletion of CD169+ macrophages in CD169-ditheria toxin receptor (CD169-DTR) mice inhibits IMQ-induced psoriasis, resulting in milder symptoms, diminished proinflammatory cytokine levels and reduced proportion of Th17 cells within the skin lesions. Furthermore, transcriptomic analysis uncovers enhanced activity in CD169+ macrophages when compared with CD169- macrophages, characterized by upregulated genes that are associated with cell activation and cell metabolism. Mechanistically, CD169+ macrophages isolated from IMQ-induced skin lesions produce more proinflammatory cytokines and exhibit enhanced ability to promote Th17 cell differentiation in vitro. Collectively, our findings highlight the crucial involvement of CD169+ macrophages in psoriasis development and offer novel insights into the heterogeneity of skin macrophages in the context of psoriasis.

An extensive investigation explores the complex terrain of psoriasis, a persistent inflammatory dermatological disorder that impacts between 1% and 3% of the worldwide populace. Acknowledging the intricate interplay between environmental, genetic, and immunological influences on the etiology of psoriasis, the study utilizes sophisticated bibliometric techniques to investigate patterns, gaps in knowledge, and emergent trends within the field. The study utilizes advanced bibliometric techniques to analyze patterns, gaps in knowledge, and emerging trends in the field while acknowledging the intricate interplay between environmental, genetic, and immune-related influences on the etiology of psoriasis. An examination of 18,765 documents from December 2012 to December 2023 was conducted using machine learning techniques and the Scopus database. The explanation for conducting analysis is rooted in its capacity to provide significant perspectives on the dynamic progression of psoriasis research. The study facilitates the identification of significant subject areas, exposes patterns in publication trends, emphasizes influential authors and journals, and outlines the worldwide contributions to the field. The study demonstrates a steady and progressive increase in publications, with significant contributions from the Journal of the American Academy of Dermatology, the British Journal of Dermatology, and the Journal of the European Academy of Dermatology and Venereology. Prominent scholars in research output, such as the United States, China, and Germany, as well as authors including Feldman, Wu, Griffiths, Puig, and Reich K., are identified. Biochemistry, genetics, and molecular biology come to the forefront as esteemed fields that make substantial contributions to the study of psoriasis alongside medicine. This research highlights the interdisciplinary aspects of psoriasis by uncovering knowledge hubs and international collaborations between authors and organizations. The findings highlight the global reach of research on psoriasis and the importance of international cooperation.