• Celiac Disease
• Diet
• Enteric Infections
• Gluten
• Microbiota

• Celiac Disease/immunology
• Celiac Disease/microbiology
• Celiac Disease/genetics
• Humans
• Animals
• Gastrointestinal Microbiome
• Severity of Illness Index
• Risk Factors
• Genetic Predisposition to Disease
• Glutens/immunology
• Glutens/adverse effects
• Diet/adverse effects
• Disease Models, Animal

• K23 DK122127 NIDDK NIH HHS
• R01 AI168478 NIAID NIH HHS

• non-small-cell lung cancer
• cancer microenvironment
• cancer genomics
• tumour immunology

• National Key Research and Development Program of China (2021YFC2500900); Shanghai Municipal Education Commission - Gaofeng Clinical Medicine Grant (20172005); program of Shanghai Academic Research Leader from Science and Technology Commission of Shanghai Municipality (20XD1402300); Novel Interdisciplinary Research Project from Shanghai Municipal Health Commission (2022JC023), Interdisciplinary Program of Shanghai Jiao Tong University (YG2023ZD04), and Clinical Research Project in Health Services of Shanghai Municipal Health Commission (202240089).

• allogeneic transplantation
• grafts
• ischemia–reperfusion injury
• mice
• neutrophils
• subsets

• 31930041 National Natural Science Foundation of China
• 32330037 National Natural Science Foundation of China

• Humans
• Nucleotidyltransferases/genetics
• Nucleotidyltransferases/metabolism
• Interferon Type I/metabolism
• DNA/metabolism
• Neoplasms/therapy
• Immunotherapy
• Immunologic Factors
• Adjuvants, Immunologic
• Autoimmune Diseases
• Communicable Diseases
• Hydrogels

• R01 AI168684 NIAID NIH HHS
• R01 CA266981 NCI NIH HHS
• R35 GM143014 NIGMS NIH HHS

• Bacillus subtilis natto
• GroEL
• IL-10
• THP-1 DC
• chaperon protein
• immunomodulatory effect

• Allergic rhinitis (AR)
• FOXD3-AS1
• Th1/Th2 cell
• dendritic cell

Immunotherapies, such as immune-checkpoint blockade and adoptive T-cell therapy, offer novel treatment options with good efficacy for patients with urothelial bladder cancer. However, heterogeneity and therapeutic resistance have limited the use of immunotherapy. Further research into immune-regulatory mechanisms in bladder cancer is urgently required. Emerging evidence demonstrates that the commensal microbiota and its interactions with host immunity play pivotal roles in a variety of physiological and pathological processes, including in cancer. The gut microbiota has been identified as a potentially effective target of treatment that can be synergized with immunotherapy. The urothelial tract is also a key site for multiple microbes, although the immune-regulatory role of the urinary microbiome in the process of carcinogenesis of bladder cancer remains to be elucidated. We performed a comprehensive analysis of the expression and biological functions of C-type lectin receptors (CLRs), which have been recognized as innate pathogen-associated receptors for fungal microbiota, in bladder cancer. In line with previous research on fungal colonization of the urothelial tract, we found that CLRs, including Dectin-1, Dectin-2, Dectin-3, and macrophage-inducible Ca²⁺-dependent lectin receptor (Mincle), had a significant association with immune infiltration in bladder cancer. Multiple innate and adaptive pathways are positively correlated with the upregulation of CLRs. In addition, we found a significant correlation between the expression of CLRs and a range of immune-checkpoint proteins in bladder cancer. Based on previous studies and our findings, we hypothesize that the urinary mycobiome plays a key role in the pathogenesis of bladder cancer and call for more research on CLR-mediated anti-fungal immunity against bladder cancer as a novel target for immunotherapy in urothelial bladder cancer.

• Antifungal Agents
• Carcinoma, Transitional Cell
• Humans
• Immune Checkpoint Inhibitors
• Immunologic Factors
• Immunotherapy
• Lectins, C-Type/metabolism
• Receptors, Mitogen
• Urinary Bladder Neoplasms/therapy

• National Natural Science Foundation of China

• Differentially expressed genes
• Gill morphology
• Osmoregulation mechanisms
• Salinity stress
• Transcriptomic analysis

• Animals
• Fishes
• Flounder/physiology
• Gills/metabolism
• Homeostasis
• Salinity
• Transcriptome
• Water/metabolism

Current organ transplantation therapy is life-saving but accompanied by well-recognized side effects due to post-transplantation systematic immunosuppressive treatment. Dendritic cells (DCs) are central instigators and regulators of transplantation immunity and are responsible for balancing allograft rejection and tolerance. They are derived from monocyte-macrophage DC progenitors originating in the bone marrow and are classified into different subsets based on their developmental, phenotypical, and functional criteria. Functionally, DCs instigate allograft immunity by presenting donor antigens to alloreactive T cells via direct, indirect, and semidirect recognition pathways and provide essential signaling for alloreactive T cell activation via costimulatory molecules and pro-inflammatory cytokines. Regulatory DCs (DCregs) are characterized by a relatively low expression of major histocompatibility complex, costimulatory molecules, and altered cytokine production and exert their regulatory function through T cell anergy, T cell deletion, and regulatory T cell induction. In rodent transplantation studies, DCreg-based therapy, by in situ targeting or infusion of ex vivo generated DCregs, exhibits promising potential as a natural, well-tolerated, organ-specific therapeutic strategy for promoting lasting organ-specific transplantation tolerance. Recent early-phase studies of DCregs have begun to examine the safety and efficacy of DCreg-induced allograft tolerance in living-donor renal or liver transplantations. The present review summarizes the basic characteristics, function, and translation of DCregs in transplantation tolerance induction.

• T cell
• allograft
• dendritic cell
• tolerance
• transplantation

Defensins represents an integral part of the innate immune system serving to ward off potential pathogens and to protect the intestinal barrier from microbial encroachment. In addition to their antimicrobial activities, defensins in general, and human β-defensin 2 (hBD2) in particular, also exhibit immunomodulatory capabilities. In this report, we assessed the therapeutic efficacy of systemically administered recombinant hBD2 to ameliorate intestinal inflammation in three distinct animal models of inflammatory bowel disease; i.e., chemically induced mucosal injury (DSS), loss of mucosal tolerance (TNBS), and T-cell transfer into immunodeficient recipient mice. Treatment efficacy was confirmed in all tested models, where systemically administered hBD2 mitigated inflammation, improved disease activity index, and hindered colitis-induced body weight loss on par with anti-TNF-α and steroids. Treatment of lipopolysaccharide (LPS)-activated human peripheral blood mononuclear cells with rhBD2 confirmed the immunomodulatory capacity in the circulatory compartment. Subsequent analyzes revealed dendritic cells (DCs) as the main target population. Suppression of LPS-induced inflammation was dependent on chemokine receptor 2 (CCR2) expression. Mechanistically, hBD2 engaged with CCR2 on its DC target cell to decrease NF-κB, and increase CREB phosphorylation, hence curbing inflammation. To our knowledge, this is the first study showing in vivo efficacy of a systemically administered defensin in experimental disease.

• IBD
• antimicrobial peptides
• host defense peptides
• innate immunity
• β-defensins

• celiac
• gluten
• infection
• microbiota
• virus

The ubiquitin-proteasome system is elementary for cellular protein degradation and gained rising attention as a new target for cancer therapy due to promising clinical trials with bortezomib, the first-in class proteasome inhibitor meanwhile approved for multiple myeloma and mantle cell lymphoma. Both bortezomib and next-generation proteasome inhibitors mediate their effects by targeting the 20S core particle of the 26S proteasome. The novel small molecule inhibitor b-AP15 affects upstream elements of the ubiquitin-proteasome cascade by suppressing the deubiquitinase activity of both proteasomal regulatory 19S subunits and showed promising anticancer activity in preclinical models. Nonetheless, effects of inhibitors on the ubiquitin-proteasome system are not exclusively restricted to malignant cells: alteration of natural killer cell-mediated immune responses had already been described for drugs targeting either 19S or 20S proteasomal subunits. Moreover, it has been shown that bortezomib impairs dendritic cell (DC) phenotype and function at different levels. In the present study, we comparatively analyzed effects of bortezomib and b-AP15 on monocyte-derived DCs. In line with previous results, bortezomib exposure impaired maturation, antigen uptake, migration, cytokine secretion and immunostimulation, whereas treatment with b-AP15 had no compromising effects on these DC features. Our findings warrant the further investigation of b-AP15 as an alternative to clinically approved proteasome inhibitors in the therapy of malignancies, especially in the context of combinatorial treatment with DC-based immunotherapies.

Dendritic cells (DCs) are key players of the immune system and thus a target for immune evasion by pathogens. We recently showed that the virulence factors phenol-soluble-modulins (PSMs) produced by community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) strains induce tolerogenic DCs upon Toll-like receptor activation via the p38-CREB-IL-10 pathway in vitro. Here, we addressed the hypothesis that S. aureus PSMs disturb the adaptive immune response via modulation of DC subsets in vivo. Using a systemic mouse infection model we found that S. aureus reduced the numbers of splenic DC subsets, mainly CD4⁺ and CD8⁺ DCs independently of PSM secretion. S. aureus infection induced upregulation of the C-C motif chemokine receptor 7 (CCR7) on the surface of all DC subsets, on CD4⁺ DCs in a PSM-dependent manner, together with increased expression of MHCII, CD86, CD80, CD40, and the co-inhibitory molecule PD-L2, with only minor effects of PSMs. Moreover, PSMs increased IL-10 production in the spleen and impaired TNF production by CD4⁺ DCs. Besides, S. aureus PSMs reduced the number of CD4⁺ T cells in the spleen, whereas CD4⁺CD25⁺Foxp3⁺ regulatory T cells (T_regs) were increased. In contrast, Th1 and Th17 priming and IFN-γ production by CD8⁺ T cells were impaired by S. aureus PSMs. Thus, PSMs from highly virulent S. aureus strains modulate the adaptive immune response in the direction of tolerance by affecting DC functions.

• Staphylococcus aureus
• T cells
• adaptive immunity
• dendritic cells
• mouse infection
• phenol-soluble modulins

• Adaptive immune response
• Environmental salinity
• Immune-related genes
• RNA-seq

• Acclimatization
• Adaptive Immunity/genetics
• Anguilla/genetics
• Anguilla/immunology
• Anguilla/metabolism
• Animals
• Computational Biology
• Fish Proteins/genetics
• Fish Proteins/immunology
• Fish Proteins/metabolism
• Gene Expression Regulation/immunology
• Gills/immunology
• Gills/metabolism
• Immunohistochemistry/veterinary
• Real-Time Polymerase Chain Reaction/veterinary
• Salinity

• Cells, Cultured
• Cytokines/analysis
• Cytokines/metabolism
• Equipment Design
• Fluorescent Dyes
• Humans
• Immunoassay/instrumentation
• Lab-On-A-Chip Devices
• Leukocytes, Mononuclear/metabolism
• Microfluidic Analytical Techniques/instrumentation
• Microspheres

• UL1 TR001445 NCATS NIH HHS

• Celiac disease
• Gluten-free diet
• Non-celiac gluten sensitivity
• Oral tolerance
• Pathogenesis

• Innate immunity
• Liver disease
• Pathophysiology
• Signaling
• Toll-like receptors

• IL-10
• PSM
• Staphylococcus aureus
• TLR
• Tolerogenic DC
• p38

• Celiac disease
• Dysbiosis
• Immune tolerance
• Innate immunity
• Interferons
• Interleukin-15
• Microbiota

• Celiac Disease/immunology
• Glutens/immunology
• Humans
• Immunity, Innate/immunology
• Interferon-alpha/immunology
• Self Tolerance/immunology

• UL1 TR000430 NCATS NIH HHS
• R01 DK067180 NIDDK NIH HHS
• P30 DK042086 NIDDK NIH HHS
• DK42086 NIDDK NIH HHS
• R01DK098435 NIDDK NIH HHS
• T32 AI007090 NIAID NIH HHS
• R01DK67180 NIDDK NIH HHS
• R01 DK098435 NIDDK NIH HHS

Objective. Helicobacter pylori (Hp) is recognized by TLR4 and TLR2 receptors, which trigger the activation of genes involved in the host immune response. Thus, we evaluated the effect of eradication therapy on TLR2 and TLR4 mRNA and protein expression in H. pylori-infected chronic gastritis patients (CG-Hp+) and 3 months after treatment. Methods. A total of 37 patients CG-Hp+ were evaluated. The relative quantification (RQ) of mRNA was assessed by TaqMan assay and protein expression by immunohistochemistry. Results. Before treatment both TLR2 and TLR4 mRNA in CG-Hp+ patients were slightly increased (TLR2 = 1.32; TLR4 = 1.26) in relation to Hp-negative normal gastric mucosa (P ≤ 0.05). After successful eradication therapy no significant change was observed (TLR2 = 1.47; TLR4 = 1.53; P > 0.05). In addition, the cagA and vacA bacterial genotypes did not influence the gene expression levels, and we observed a positive correlation between the RQ values of TLR2 and TLR4, both before and after treatment. Immunoexpression of the TLR2 and TLR4 proteins confirmed the gene expression results. Conclusion. In conclusion, the expression of both TLR2 and TLR4 is increased in CG-Hp+ patients regardless of cagA and vacA status and this expression pattern is not significantly changed after eradication of bacteria, at least for the short period of time evaluated.

The endotoxic portion of lipopolysaccharide (LPS), a glycophospholipid Lipid A, initiates the activation of the Toll-like Receptor 4 (TLR4)–myeloid differentiation factor 2 (MD-2) complex, which results in pro-inflammatory immune signaling. To unveil the structural requirements for TLR4·MD-2-specific ligands, we have developed conformationally restricted Lipid A mimetics wherein the flexible βGlcN(1→6)GlcN backbone of Lipid A is exchanged for a rigid trehalose-like αGlcN(1↔1)αMan scaffold resembling the molecular shape of TLR4·MD-2-bound E. coli Lipid A disclosed in the X-ray structure. A convergent synthetic route toward orthogonally protected αGlcN(1↔1)αMan disaccharide has been elaborated. The α,α-(1↔1) linkage was attained by the glycosylation of 2-N-carbamate-protected α-GlcN-lactol with N-phenyl-trifluoroacetimidate of 2-O-methylated mannose. Regioselective acylation with (R)-3-acyloxyacyl fatty acids and successive phosphorylation followed by global deprotection afforded bis- and monophosphorylated hexaacylated Lipid A mimetics. αGlcN(1↔1)αMan-based Lipid A mimetics (α,α-GM-LAM) induced potent activation of NF-κB signaling in hTLR4/hMD-2/CD14-transfected HEK293 cells and robust LPS-like cytokines expression in macrophages and dendritic cells. Thus, restricting the conformational flexibility of Lipid A by fixing the molecular shape of its carbohydrate backbone in the “agonistic” conformation attained by a rigid αGlcN(1↔1)αMan scaffold represents an efficient approach toward powerful and adjustable TLR4 activation.

High mobility group box 1 protein (HMGB1), as a mediator of late inflammation, provides a wide therapeutic window. Extracellular HMGB1 as an endogenous injury-related molecule promotes the development of inflammation and damage by binding to its receptors. Studies have discovered that lipopolysaccharide and vacuolating cytotoxin A (VacA) of Helicobacter pylori (H. pylori) are strong stimulating factors of HMGB1 expression, and its extracellular receptors Toll-like receptors (TLRs) are closely associated with H. pylori infection and pathogenicity. Therefore, the HMGB1/TLR signaling pathway may play an important role in inflammatory response and immune abnormalities caused by H. pylori infection. This article will discuss the role of the HMGB1/TLR signaling pathway in H. pylori infection.

• High mobility group box 1 protein
• Helicobacter pylori
• Toll-like receptor
• Inflammatory response
• Immune abnormality

• IL-12
• Th1
• dendritic cell
• p38
• signaling

• Cryptosporidium parvum
• dendritic cell
• mesenteric lymph node

• biomedical applications
• cell separation
• immune cell
• immunophenotyping
• microfluidics

• Dimethylpolysiloxanes
• Filtration/instrumentation
• Humans
• Immunophenotyping
• Lymphocytes/cytology
• Membranes, Artificial
• Monocytes/cytology
• Surface Properties

• R01 HL119542 NHLBI NIH HHS
• R01HL097361 NHLBI NIH HHS
• K08HD062142 NICHD NIH HHS
• R01 HL097361 NHLBI NIH HHS
• UL1 RR024986 NCRR NIH HHS
• K12HD047349 NICHD NIH HHS
• UL1RR024986 NCRR NIH HHS
• K08 HD062142 NICHD NIH HHS
• K12 HD047349 NICHD NIH HHS

• immunophenotyping
• microfluidics

• Asthma/genetics
• Asthma/metabolism
• Case-Control Studies
• Child
• Gene Frequency
• Humans
• Linkage Disequilibrium
• Polymorphism, Single Nucleotide
• Signal Transduction
• Toll-Like Receptors/genetics
• Toll-Like Receptors/metabolism

Dendritic cells (DC) are critical to an integrated immune response and serve as the key link between the innate and adaptive arms of the immune system. Under steady state conditions, brain DC’s act as sentinels, continually sampling their local environment. They share this function with macrophages derived from the same basic hemopoietic (bone marrow-derived) precursor and with parenchymal microglia that arise from a unique non-hemopoietic origin. While multiple cells may serve as antigen presenting cells (APCs), dendritic cells present both foreign and self-proteins to naïve T cells that, in turn, carry out effector functions that serve to protect or destroy. The resulting activation of the adaptive response is a critical step to resolution of injury or infection and is key to survival. In this review we will explore the critical roles that DCs play in the brain’s response to neuroinflammatory disease with emphasis on how the brain’s microenvironment impacts these actions.

We recently isolated and identified Zizimin2 as a functional factor that is highly expressed in murine splenic germinal center B cells after immunization with T-cell-dependent antigen. Zizimin2 was revealed to be a new family member of Dock (dedicator of cytokinesis), Dock11, which is the guanine nucleotide exchange factor for Cdc42, a low-molecular-weight GTPase. However, the molecular function of Zizimin2 in acquired immunity has not been elucidated.

In this study, we show that the protein expression of Zizimin2, which is also restricted to lymphoid tissues and lymphocytes, is reduced in aged mice. Over-expression of full-length Zizimin2 induced filopodial formation in 293T cells, whereas expression of CZH2 domain inhibited it. Stimulation of Fcγ receptor and Toll-like receptor 4 triggered Zizimin2 up-regulation and Cdc42 activation in bone marrow-derived dendritic cells.

These data suggest that Zizimin2 is an immune-related and age-regulated guanine nucleotide exchange factor, which facilitates filopodial formation through activation of Cdc42, which results in activation of cell migration.

There is a growing need for novel vaccine adjuvants that can provide safe and potent T-helper type 1 (Th1) activity. RNA-like immune response modifiers (IRMs) are candidate T-cell adjuvants that skew acquired immune responses towards a Th1 phenotype. We set out to delineate the essential signaling pathways by which the RNA-like IRMs, resiquimod (R-848) and polyinosinic:polycytidylic acid (poly I:C), augment CD4+ T-helper 1 (Th1) responses. Highly purified murine conventional dendritic cells (cDCs) and conventional CD4+ T-cells were co-cultured in allogeneic and MHC congenic mixed leukocyte reactions. The activation of CD4+ Th1 cells was examined utilizing cells from mice deficient in specific RNA-sensing pattern recognition receptors and signaling mediators. R-848 and poly I:C stimulation of Type I interferon production and signaling in cDCs was essential but not sufficient for driving CD4+ Th1 responses. The early and rapid production of IL-1α and IL-1β was equally critical for the optimal activation of Th1 CD4+ T-cells. R-848 activation of Toll-like receptor 7/MyD88-dependent signaling in cDCs led to a rapid upregulation of pro-IL-1α and pro-IL-1β production compared to poly I:C activation of MyD88-independent signaling pathways. The in vitro data show that CD4+ T-cell adjuvant activity of RNA-like IRMs is mediated by a critical combination of early and rapid Type I interferon, IL-1α and IL-1β production. These results provide important insights into the key signaling pathways responsible for RNA-like IRM CD4+ Th1 activation. A better understanding of the critical signaling pathways by which RNA-like IRMs stimulate CD4+ Th1 responses is relevant to the rational design of improved vaccine adjuvants.

• Adjuvants, Immunologic/chemistry
• Adjuvants, Immunologic/pharmacology
• Animals
• CD4-Positive T-Lymphocytes/cytology
• CD4-Positive T-Lymphocytes/drug effects
• CD4-Positive T-Lymphocytes/immunology
• CD4-Positive T-Lymphocytes/metabolism
• Dendritic Cells/drug effects
• Dendritic Cells/immunology
• Dendritic Cells/metabolism
• Imidazoles/chemistry
• Imidazoles/pharmacology
• Interferon Type I/biosynthesis
• Interferon Type I/metabolism
• Interleukin-1alpha/biosynthesis
• Interleukin-1alpha/genetics
• Interleukin-1alpha/metabolism
• Interleukin-1beta/biosynthesis
• Interleukin-1beta/genetics
• Interleukin-1beta/metabolism
• Mice
• Myeloid Differentiation Factor 88/metabolism
• Poly I-C/chemistry
• Poly I-C/pharmacology
• RNA/chemistry
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Signal Transduction/drug effects
• Signal Transduction/immunology
• Th1 Cells/cytology
• Th1 Cells/drug effects
• Th1 Cells/immunology
• Th1 Cells/metabolism
• Time Factors

• U19 AI057319 NIAID NIH HHS
• U19 AI57319 NIAID NIH HHS

• Antigens, Surface/analysis
• Blood Donors
• Cells, Cultured
• Cytokines/administration & dosage
• Cytokines/immunology
• Dendritic Cells/chemistry
• Dendritic Cells/drug effects
• Dendritic Cells/immunology
• Humans
• Immunotherapy/methods
• Lipid A/administration & dosage
• Lipid A/analogs & derivatives
• Lipid A/immunology

• Antigens, CD/analysis
• Antigens, CD/immunology
• B7-1 Antigen/analysis
• B7-1 Antigen/immunology
• CD4-Positive T-Lymphocytes/drug effects
• CD4-Positive T-Lymphocytes/immunology
• CD40 Antigens/analysis
• CD40 Antigens/immunology
• Cell Differentiation/drug effects
• Cell Differentiation/immunology
• Cells, Cultured
• Coculture Techniques
• Dendritic Cells/drug effects
• Dendritic Cells/immunology
• Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
• Guanosine/analogs & derivatives
• Guanosine/pharmacology
• Humans
• Immunoglobulins/analysis
• Immunoglobulins/immunology
• Intercellular Adhesion Molecule-1/analysis
• Intercellular Adhesion Molecule-1/immunology
• Interferon-gamma/analysis
• Interferon-gamma/immunology
• Interferon-gamma/metabolism
• Interleukin-4/immunology
• Interleukin-4/pharmacology
• Interleukins/analysis
• Interleukins/biosynthesis
• Interleukins/immunology
• Leukocytes, Mononuclear/immunology
• Leukocytes, Mononuclear/metabolism
• Membrane Glycoproteins/analysis
• Membrane Glycoproteins/immunology
• Receptors, CCR7/analysis
• Receptors, CCR7/immunology
• Recombinant Proteins
• Th1 Cells/drug effects
• Th1 Cells/immunology
• Th17 Cells/drug effects
• Th17 Cells/immunology
• Toll-Like Receptor 7/agonists
• Toll-Like Receptor 7/analysis
• Toll-Like Receptor 7/immunology
• Up-Regulation
• CD83 Antigen

• Animals
• Antigen Presentation
• Cell Communication
• Dendritic Cells/cytology
• Dendritic Cells/immunology
• Humans
• Immune Tolerance
• Mice
• T-Lymphocytes, Regulatory/cytology
• T-Lymphocytes, Regulatory/immunology

• AR42689 NIAMS NIH HHS
• HL56949 NHLBI NIH HHS
• AI078897 NIAID NIH HHS
• P30 AR042689 NIAMS NIH HHS
• P01 AI078897 NIAID NIH HHS
• AI069259 NIAID NIH HHS
• P01 HL056949 NHLBI NIH HHS
• AI072252 NIAID NIH HHS
• R01 AI072252 NIAID NIH HHS
• R01 AI069259 NIAID NIH HHS

• cytokines
• dendritic cells
• toll-like receptors

• Antigens, CD34/analysis
• Cell Differentiation/immunology
• Cells, Cultured
• Cytokines/metabolism
• HLA-DR Antigens/biosynthesis
• Humans
• Immunophenotyping
• Langerhans Cells/cytology
• Langerhans Cells/immunology
• Ligands
• RNA, Messenger/genetics
• Reverse Transcriptase Polymerase Chain Reaction/methods
• Stem Cells/cytology
• Stem Cells/immunology
• Toll-Like Receptors/metabolism
• Tumor Necrosis Factor-alpha/immunology
• Up-Regulation/immunology

• G0100482 Medical Research Council

• b cells
• ap-1
• jnk
• cd40
• tlr7

• Adult
• Animals
• B-Lymphocytes/immunology
• CD40 Antigens/physiology
• Cell Line, Tumor
• Cells, Cultured
• Cytokines/biosynthesis
• Humans
• Interleukin-6/biosynthesis
• JNK Mitogen-Activated Protein Kinases/metabolism
• JNK Mitogen-Activated Protein Kinases/physiology
• Lymphocyte Activation/immunology
• Membrane Glycoproteins/physiology
• Mice
• Mice, Inbred C57BL
• Signal Transduction/immunology
• Toll-Like Receptor 7/physiology
• Toll-Like Receptor 8/physiology
• Transcription Factor AP-1/metabolism
• Transcription Factor AP-1/physiology

• R01 CA099997 NCI NIH HHS
• R56 AI049993 NIAID NIH HHS
• R01 AI028847 NIAID NIH HHS
• CA 099997 NCI NIH HHS
• R56 AI028847 NIAID NIH HHS
• R01 AI049993 NIAID NIH HHS
• AI 49993 NIAID NIH HHS
• AI 28847 NIAID NIH HHS