• Immune cells(2)
• Machine learning(5)
• Pathological structure(3)
• Tuberculosis granulomas(1)
• cytokines(4)

• Humans
• Tuberculosis, Pulmonary/immunology
• Tuberculosis, Pulmonary/pathology
• Tuberculosis, Pulmonary/genetics
• Tuberculosis, Pulmonary/microbiology
• Computational Biology
• Cytokines/immunology
• Cytokines/genetics
• Cytokines/blood
• Mycobacterium tuberculosis/immunology
• Mycobacterium tuberculosis/pathogenicity
• Transcriptome
• Granuloma/immunology
• Granuloma/microbiology
• Granuloma/genetics
• Granuloma/pathology
• Case-Control Studies
• Granuloma, Respiratory Tract/immunology
• Granuloma, Respiratory Tract/genetics
• Granuloma, Respiratory Tract/microbiology
• Granuloma, Respiratory Tract/pathology
• Male
• Female
• Adult
• Host-Pathogen Interactions
• Single-Cell Analysis
• Middle Aged
• Lung/immunology
• Lung/microbiology
• Lung/pathology

• T-lymphocytes
• healthy subjects
• immune aging
• meta-analysis
• systematic review

• Humans
• Homeostasis/immunology
• T-Lymphocyte Subsets/immunology
• Aging/immunology
• Age Factors
• T-Lymphocytes/immunology
• Lymphocyte Count
• Adult
• Immunologic Memory
• Infant

• Russian Science Foundation
• Ministry of Education and Science of the Russian Federation

• CD4+ T-lymphocytopenia
• Interleukin-6
• Interleukin-8
• Meningeal
• Predictive value
• Tuberculosis

• anti-interferon-gamma autoantibody-associated adult-onset immunodeficiency (AOID) syndrome
• bortezomib
• efficacy
• opportunistic infection
• treating

• Adult
• Humans
• Middle Aged
• Autoantibodies
• Bortezomib/adverse effects
• Thailand
• Interferon-gamma
• Immunologic Deficiency Syndromes/drug therapy
• Immunologic Deficiency Syndromes/complications
• Cyclophosphamide/therapeutic use

• 61-049 Health Systems Research Institute

• apoptosis
• chronic infection
• hematopoiesis
• lymphopenia
• tuberculosis

• 82001675 Youth Science Fund Project of the National Natural Science Foundation of China
• 23JRRA1100 Gansu Science and Technology Project of China
• lzujbky-2023-17 Fundamental Research Funds for the Central Universities of the Lanzhou University

• Cytokine production
• Functional T cell analysis
• Immunodeficiency
• Interferon gamma receptor
• Mycobacterium avium complex infections

• Adult
• Humans
• Female
• Mycobacterium avium Complex/genetics
• Mycobacterium avium Complex/metabolism
• Leukocytes, Mononuclear
• Mycobacterium avium-intracellulare Infection/genetics
• Mycobacterium avium-intracellulare Infection/metabolism
• Cytokines/metabolism
• Lymphadenitis/metabolism

• HIV
• antiretroviral therapy
• immune aging
• sCD14

• Mycobacterium tuberculosis
• children
• humoral immunity
• immunoglobulins
• selective IgA deficiency
• selective IgM deficiency
• tuberculosis

• Flow cytometry
• Sputum culture conversion
• Tuberculosis
• sICAM-1
• suPAR

• Mtb
• Mycobacterium
• PBMC
• T regulatory cells
• immune responses
• microbiology

Easily accessible tools that reliably stratify Mycobacterium tuberculosis (MTB) infection are needed to facilitate the improvement of clinical management. The current study attempts to reveal lymphocyte-related immune characteristics of active tuberculosis (ATB) patients and establish immunodiagnostic model for discriminating ATB from latent tuberculosis infection (LTBI) and healthy controls (HC).

A total of 171 subjects consisted of 54 ATB, 57 LTBI, and 60 HC were consecutively recruited at Tongji hospital from January 2019 to January 2021. All participants were tested for lymphocyte subsets, phenotype, and function. Other examination including T-SPOT and microbiological detection for MTB were performed simultaneously.

Compared with LTBI and HC, ATB patients exhibited significantly lower number and function of lymphocytes including CD4⁺ T cells, CD8⁺ T cells and NK cells, and significantly higher T cell activation represented by HLA-DR and proportion of immunosuppressive cells represented by Treg. An immunodiagnostic model based on the combination of NK cell number, HLA-DR⁺CD3⁺ T cells, Treg, CD4⁺ T cell function, and NK cell function was built using logistic regression. Based on receiver operating characteristic curve analysis, the area under the curve (AUC) of the diagnostic model was 0.920 (95% CI, 0.867-0.973) in distinguishing ATB from LTBI, while the cut-off value of 0.676 produced a sensitivity of 81.48% (95% CI, 69.16%-89.62%) and specificity of 91.23% (95% CI, 81.06%-96.20%). Meanwhile, AUC analysis between ATB and HC according to the diagnostic model was 0.911 (95% CI, 0.855-0.967), with a sensitivity of 81.48% (95% CI, 69.16%-89.62%) and a specificity of 90.00% (95% CI, 79.85%-95.34%).

Our study demonstrated that the immunodiagnostic model established by the combination of lymphocyte-related indicators could facilitate the status differentiation of MTB infection.

• active tuberculosis
• differential diagnosis
• immunodiagnostic model
• immunological biomarkers
• latent tuberculosis infection
• lymphocyte

Patients with systemic lupus erythematosus (SLE) suffer frequent infections that account for significant morbidity and mortality. T cell cytotoxic responses are decreased in patients with SLE, yet the responsible molecular events are largely unknown. We find an expanded CD8CD38^high T cell subset in a sub-group of patients with increased rates of infections. CD8CD38^high T cells from healthy subjects and patients with SLE display decreased cytotoxic capacity, degranulation, and expression of granzymes A and B and perforin. The key cytotoxicity-related transcription factors T-bet, RUNX3, and EOMES are decreased in CD8CD38^high T cells. CD38 leads to increased acetylated EZH2 through inhibition of the deacetylase Sirtuin1. Acetylated EZH2 represses RUNX3 expression, whereas inhibition of EZH2 restores CD8 T cell cytotoxic responses. We propose that high levels of CD38 lead to decreased CD8 T cell-mediated cytotoxicity and increased propensity to infections in patients with SLE, a process that can be reversed pharmacologically.

Katsuyama et al. find that an expanded CD8CD38^high T cell population in SLE patients is linked to infections. CD8CD38^high T cells display decreased cytotoxic capacity by suppressing the expression of related molecules through an NAD⁺/Sirtuin1/EZH2 pathway. EZH2 inhibitors increase cytotoxicity offering a means to mitigate infection rates in SLE.

• CD38
• CD8 T cell
• EZH2
• Sirtuin1
• cytotoxicity
• infection
• nicotinamide adenine dinucleotide
• patients
• systemic lupus erythematosus

• Diabetes
• Monocytes
• Natural killer cells
• T cells

The lack of efficient tools for identifying immunological correlates of tuberculosis (TB) protection or risk of disease progression impedes the development of improved control strategies. To more clearly understand the host response in TB, we recently established an imaging flow cytometer‐based in‐vitro assay, which assesses multiple aspects of T cell–monocyte interaction. Here, we extended our previous work and characterized communication between T cells and monocytes using clinical samples from individuals with different TB infection status and healthy controls from a TB endemic setting. To identify T cell–monocyte conjugates, peripheral blood mononuclear cells (PBMC) were stimulated with ds‐Red‐expressing Mycobacterium bovis bacille Calmette–Guérin or 6‐kDa early secreted antigenic target (ESAT 6) peptides for 6 h, and analyzed by imaging flow cytometer (IFC). We then enumerated T cell–monocyte conjugates using polarization of T cell receptor (TCR) and F‐actin as markers for synapse formation, and nuclear factor kappa B (NF‐κB) nuclear translocation in the T cells. We observed a reduced frequency of T cell–monocyte conjugates in cells from patients with active pulmonary tuberculosis (pTB) compared to latent TB‐infected (LTBI) and healthy controls. When we monitored NF‐κB nuclear translocation in T cells interacting with monocytes, the proportion of responding cells was significantly higher in active pTB compared with LTBI and controls. Overall, these data underscore the need to consider multiple immunological parameters against TB, where IFC could be a valuable tool.

• T cell
• cell activation
• monocyte

• Cytokines
• immunity
• natural killer cell
• regulatory T cell

• IL-2
• Mycobacterium tuberculosis
• T cell dysfunction
• T cell exhaustion
• antigen persistence

Pathogenesis of mycobacterial infection has been extensively studied determining the fundamental role of host immunocompetence in disease progression. Cellular adaptive immunity, in particular CD4+ cells, has shown to be crucial in the host defence. A role of cytotoxic lymphocytes and humoral immunity has also been established. However, few studies have been performed in low endemic countries on immunological correlates of tuberculosis in paediatric patients. The present study aims to fill this gap analysing the distribution and the absolute values of the main lymphocyte subpopulations (CD3+, CD4+, CD8+, CD19+ and CD16+/CD56+) in the different stages of tubercular infection in human immunodeficiency virus–negative children living in low tubercular endemic countries. Results obtained in children with latent tuberculosis, active tuberculosis and healthy controls were compared. Moreover, quantitative analysis of interferon-γ levels of mitogen-induced response was carried out within the different study groups. The aim of this analysis was to enforce the comprehension of immune modifications subsequent to Mycobacterium tuberculosis infection. The major finding of our study was CD3+ and CD4+ absolute and percentage depletion in children with active tuberculosis versus healthy controls. Moreover, severe forms of active tuberculosis showed a marked reduction in the CD4+ percentage in the context of a systemic impairment which affects globally the absolute count of all peripheral lymphocyte subsets tested. A relative increase of natural killer cells was proved in infected patients, whereas no differences in B cells among the study groups were detected. Mitogen-induced interferon-γ levels were significantly higher in children with latent tuberculosis when compared to active tuberculosis and healthy controls, demonstrating effective immune activation in those patients able to control the infection.

• CD4+
• interferon
• lymphocyte subsets
• paediatric
• tuberculosis

• Adolescent
• Antigens, CD19/blood
• CD3 Complex/blood
• CD4-Positive T-Lymphocytes/metabolism
• CD56 Antigen/blood
• CD8-Positive T-Lymphocytes/metabolism
• Child
• Child, Preschool
• Cross-Sectional Studies
• GPI-Linked Proteins/blood
• Humans
• Male
• Receptors, IgG/blood
• Tuberculosis/blood
• Tuberculosis/diagnosis

• HIV
• T cell activation
• memory T cell
• naïve T cell
• tuberculosis

Lymph node tuberculosis (LNTB) is the most frequent extrapulmonary form of tuberculosis (TB). Studies of human tuberculosis at sites of disease are limited. LNTB provides a unique opportunity to compare local in situ and peripheral blood immune response in active Mycobacterium tuberculosis (Mtb) disease. The present study analysed T regulatory cells (Treg) frequency and activation along with CD4+ T cell function in lymph nodes from LNTB patients.

Lymph node mononuclear cells (LNMC) were compared to autologous peripheral blood mononuclear cells (PBMC). LNMC were enriched for CD4+ T cells with a late differentiated effector memory phenotype. No differences were noted in the frequency and mutifunctional profile of memory CD4+ T cells specific for Mtb. The proportion of activated CD4+ and Tregs in LNMC was increased compared to PBMC. The correlation between Tregs and activated CD4+ T cells was stronger in LNMC than PBMC. Tregs in LNMC showed a strong positive correlation with Th1 cytokine production (IL2, IFNγ and TNFα) as well as MIP-1α after Mtb antigen stimulation. A subset of Tregs in LNMC co-expressed HLA-DR and CD38, markers of activation.

Further research will determine the functional relationship between Treg and activated CD4+ T cells at lymph node sites of Mtb infection.

The online version of this article (10.1186/s12865-018-0266-8) contains supplementary material, which is available to authorized users.

• Lymph node
• Lymphadenitis
• Treg cells
• Tuberculosis
• activation
• conventional T cell

• HIV patients
• Interrupted anti-retroviral treatment
• active pulmonary tuberculosis
• memory and naive T cells

• Adult
• Anti-Retroviral Agents/therapeutic use
• Antitubercular Agents/therapeutic use
• CD4 Lymphocyte Count
• CD4-Positive T-Lymphocytes/immunology
• CD8-Positive T-Lymphocytes/immunology
• Female
• Flow Cytometry
• HIV Infections/complications
• HIV Infections/drug therapy
• HIV Infections/immunology
• Humans
• Immune Reconstitution Inflammatory Syndrome/etiology
• Immunologic Memory/immunology
• Male
• Mycobacterium tuberculosis/isolation & purification
• Tuberculosis, Pulmonary/diagnosis
• Tuberculosis, Pulmonary/drug therapy
• Tuberculosis, Pulmonary/immunology
• Viral Load/immunology

• Co-stimulation
• HIV/TB co-infection
• Immune activation
• Immunosenescence
• T-cell activation

• Interferon gamma release assays
• Pathogen associated molecular patterns
• Quantiferon
• Tuberculosis

In recent years, chronic immune activation and systemic inflammation have emerged as hallmarks of HIV disease progression and mortality. Several studies indicate that soluble inflammatory biomarkers (sCD14, IL-6, IL-8, CRP and hyaluronic acid), as well as surface markers of T-cell activation (CD38, HLA-DR) independently predict progression to AIDS and mortality in HIV-infected individuals. While co-infections have been shown to contribute to immune activation, the impact of latent tuberculosis infection (LTBI), which is widely endemic in the areas most affected by the global AIDS epidemic, has not been evaluated. We hypothesized that both active and latent states of Mycobacterium tuberculosis co-infection contribute to elevated immune activation as measured by these markers. In HIV-infected individuals with active, but not latent TB, we found elevated levels of soluble markers associated with monocyte activation. Interestingly, T-cell activation was elevated individuals with both latent and active TB. These results suggest that in the highly TB- and HIV-endemic settings of southern Africa, latent TB-associated T-cell activation may contribute to HIV disease progression and exacerbate the HIV epidemic. In addition, our findings indicate that aggressive campaigns to treat LTBI in HIV-infected individuals in high-burden countries will not only impact TB rates, but may also slow HIV progression.

Latent tuberculosis, which affects an estimated 1/3 of the world's population, has long been thought to be a relatively benign, quiescent state of M. tuberculosis infection. While HIV co-infection is known to exacerbate M. tuberculosis infection and increase the risk of developing active TB, little is known about the potential effect of latent TB infection on HIV disease. This study shows that HIV-infected individuals with both active and latent TB have elevated levels of inflammation and immune activation, biomarkers of HIV disease progression and elevated risk of mortality. These results suggest that, in the context of HIV, latent TB infection may be associated with increased risk of progression to AIDS and mortality.

•

While HIV co-infection is known to exacerbate TB, little is known about the effect of latent TB infection on HIV disease.

• HIV
• immune activation
• inflammation
• tuberculosis

• ADP-ribosyl Cyclase 1/blood
• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Antitubercular Agents/therapeutic use
• Asymptomatic Diseases
• Biomarkers
• CD4-Positive T-Lymphocytes/chemistry
• Diagnosis, Differential
• Drug Monitoring
• Female
• Flow Cytometry/methods
• Georgia
• HLA-DR Antigens/blood
• Humans
• Interferon-gamma/blood
• Ki-67 Antigen/blood
• Latent Tuberculosis/blood
• Latent Tuberculosis/diagnosis
• Latent Tuberculosis/immunology
• Lymphocyte Activation
• Male
• Membrane Glycoproteins/blood
• Middle Aged
• Mycobacterium tuberculosis/immunology
• Mycobacterium tuberculosis/isolation & purification
• Sensitivity and Specificity
• South Africa
• Sputum/microbiology
• Tuberculosis, Pulmonary/blood
• Tuberculosis, Pulmonary/diagnosis
• Tuberculosis, Pulmonary/drug therapy
• Tuberculosis, Pulmonary/immunology
• Young Adult

• AI057266 NIAID NIH HHS
• P30 AI050409 NIAID NIH HHS
• RR000165 NCRR NIH HHS
• P51 OD011132 NIH HHS
• U19 AI057266 NIAID NIH HHS
• R25 TW009337 FIC NIH HHS
• R01 AI083156 NIAID NIH HHS
• P30AI050409 NIAID NIH HHS
• P51 RR000165 NCRR NIH HHS
• AI083156 NIAID NIH HHS

• QFT
• Regulatory T cells
• TST
• Tuberculosis

Immunosenescence is marked by accelerated degradation of host immune responses leading to the onset of opportunistic infections, where senescent T cells show remarkably higher ontogenic defects as compared to healthy T cells. The mechanistic association between T-cell immunosenescence and human immunodeficiency virus (HIV) disease progression, and functional T-cell responses in HIV-tuberculosis (HIV-TB) co-infection remains to be elaborately discussed. Here, we discussed the association of immunosenescence and chronic immune activation in HIV-TB co-infection and reviewed the role played by mediators of immune deterioration in HIV-TB co-infection necessitating the importance of designing therapeutic strategies against HIV disease progression and pathogenesis.

• Cluster of differentiation 38
• Human immunodeficiency virus-tuberculosis co-infection
• Immu-nosenescence

• R01 AI052731 NIAID NIH HHS
• R37 AI052731 NIAID NIH HHS

• CD4+/CD8+ Ratio
• Meta-analysis
• Pulmonary Tuberculosis

• Biosignature
• RT-MLPA
• gene expression
• tuberculosis

Tuberculosis (TB) has been shown to accelerate the clinical course of HIV infection, but the mechanisms by which this occurs are not well understood. Regulatory T-cells (Tregs) are known to dampen hyperactivation of the immune cells, but it remains unclear whether hyperactivation of T-cells in HIV infection is associated with a decrease of Tregs and what the effect Mycobacterium tuberculosis (MTB) co-infection has on T-cell activation and Tregs.

In this study, we aim to evaluate whether active TB is associated with the increased expression of T-cell activation markers and reduced number of Treg cells in HIV-1-infected patients.

This study was conducted on 69 subjects consisting of 20 HIV-infected patients, 20 HIV and MTB co-infected patients, 19 MTB-infected patients and 10 uninfected control subjects negative for both MTB and HIV. The frequencies of T-cell activation markers (CD38 and HLA-DR) and Treg cells (CD4⁺CD25⁺CD127-) were measured by flow cytometry.

Significantly higher expression of CD38 and HLA-DR on CD4⁺ and CD8⁺ T-cells was found in MTB and HIV co-infected patients compared with HIV-infected patients. However, no significant difference in the percentage of Treg cells was reported between HIV patients with TB and those without. The study also showed a negative correlation between regulatory T-cells frequency and CD4⁺ T-cell counts.

These results suggest that TB enhances the expression of peripheral T-cell activation markers during HIV infection, whilst having no impact on the percentages of Treg cells.

Tuberculosis (TB) continues to be the most frequent cause of illness and death from an infectious agent globally, and its interaction with HIV is having devastating effects. To investigate how HIV alters the immune response to Mycobacterium tuberculosis (Mtb), we assessed basal and Mtb-induced proliferation, cytokine production, and expression of signalling lymphocytic activation molecule (SLAM), inducible costimulator (ICOS) and programmed death-1 (PD-1) on T lymphocytes from HIV-positive individuals coinfected with TB, HIV-positive subjects, TB patients and healthy donors (HD).

HIV-TB patients showed increased ICOS, SLAM and PD-1 basal levels on T lymphocytes, whereas HIV-positive individuals displayed elevated levels of SLAM and PD-1, TB patients high levels of SLAM, and HD low levels of the three proteins. Mtb-stimulation enhanced ICOS expression in the four groups, but only TB and HD increased SLAM and PD-1 levels.

These data show the immune deregulation that takes place during the immune response against TB in different study populations.

• Adaptive Immunity
• Animals
• Antigens/immunology
• Bacteria/immunology
• Cytokines/analysis
• Cytokines/biosynthesis
• Cytokines/immunology
• Host-Parasite Interactions
• Host-Pathogen Interactions
• Humans
• Immunity, Innate
• Nematoda/immunology
• T-Lymphocyte Subsets/immunology
• T-Lymphocytes/immunology
• Th1-Th2 Balance
• Vaccines/immunology
• Zoonoses/microbiology
• Zoonoses/parasitology

• Adult
• Aged
• Antitubercular Agents/administration & dosage
• CD4 Antigens/analysis
• Case-Control Studies
• Forkhead Transcription Factors/analysis
• Humans
• Interleukin-2 Receptor alpha Subunit/analysis
• Interleukin-7 Receptor alpha Subunit/analysis
• Lymphocyte Activation
• Male
• Middle Aged
• Mycobacterium tuberculosis/immunology
• T-Lymphocyte Subsets/chemistry
• T-Lymphocyte Subsets/immunology
• T-Lymphocytes, Regulatory/immunology
• Tuberculosis/drug therapy
• Tuberculosis/immunology

• K23 AI091692 NIAID NIH HHS
• P30 AI054999 NIAID NIH HHS
• N01 AI065298 NIAID NIH HHS
• P30 AI 54999 NIAID NIH HHS
• K24 AI065298 NIAID NIH HHS

• tuberculosis
• pleuritis
• cd4+ t cells
• immunity
• polyfunctional

• Adolescent
• Adult
• Aged
• CD4-Positive T-Lymphocytes/immunology
• CD4-Positive T-Lymphocytes/metabolism
• Chemokine CCL3/biosynthesis
• Female
• Flow Cytometry
• Humans
• Interferon-gamma/biosynthesis
• Interleukin-2/biosynthesis
• Male
• Middle Aged
• Morocco/epidemiology
• Mycobacterium tuberculosis/cytology
• Mycobacterium tuberculosis/immunology
• Phenotype
• Tuberculosis, Pleural/epidemiology
• Tuberculosis, Pleural/genetics
• Tuberculosis, Pleural/immunology
• Tumor Necrosis Factor-alpha/biosynthesis
• Uganda/epidemiology
• Young Adult

• AI-73217 NIAID NIH HHS
• N01 AI070022 NIAID NIH HHS
• R56 HL051636 NHLBI NIH HHS
• R01 HL051636 NHLBI NIH HHS
• R21 AI073217 NIAID NIH HHS
• AI-36219 NIAID NIH HHS
• P30 AI036219 NIAID NIH HHS
• HL-51636 NHLBI NIH HHS
• R01 AI080313 NIAID NIH HHS

• Adult
• Anti-HIV Agents/administration & dosage
• Antiretroviral Therapy, Highly Active
• Antitubercular Agents/administration & dosage
• CD4 Lymphocyte Count
• Cytokines/metabolism
• Female
• HIV Infections/complications
• HIV Infections/drug therapy
• HIV Infections/immunology
• Humans
• Male
• Middle Aged
• T-Lymphocyte Subsets/immunology
• Treatment Outcome
• Tuberculosis, Pulmonary/complications
• Tuberculosis, Pulmonary/drug therapy
• Tuberculosis, Pulmonary/immunology

• K24 AI051982 NIAID NIH HHS
• HHSN266200700022C/NO1-AI-70022 NIAID NIH HHS
• K08 AI083739 NIAID NIH HHS
• L40 AI079847 NIAID NIH HHS
• AI051219 NIAID NIH HHS
• T32 HL07889 NHLBI NIH HHS
• UM1 AI069496 NIAID NIH HHS

Patients with tuberculosis frequently develop anergy, a state of T-cell hyporesponsiveness in which defective T-cell costimulation could be a factor. To know if the expression of T-cell costimulatory molecules was altered in tuberculosis, we analyzed the peripheral blood T-cell phenotype of 23 Mexican patients with pulmonary tuberculosis. There was severe CD4 (P < .001) and CD8 (P < .01) lymphopenia and upregulation of costimulatory molecule CD30 on CD4 and CD8 T cells (P < .05); this increase was higher in relapsing tuberculosis. The main finding was severe downregulation of the major costimulatory molecule CD28 on both CD8 and CD4 T cells (P < .001). Depletion of the CD4/CD28 subset, a hitherto undescribed finding, is relevant because CD4 T cells constitute the main arm of the cell-mediated antimycobacterial immune response.

• HLA-DR
• NK-T cell
• multidrug-resistant tuberculosis
• γδ T cell

• Adolescent
• Adult
• Aged
• Antigens, CD/metabolism
• B-Lymphocytes/cytology
• B-Lymphocytes/immunology
• CD4-CD8 Ratio
• CD4-Positive T-Lymphocytes/cytology
• CD4-Positive T-Lymphocytes/immunology
• CD8-Positive T-Lymphocytes/cytology
• CD8-Positive T-Lymphocytes/immunology
• Female
• Humans
• Lymphocyte Subsets/cytology
• Lymphocyte Subsets/immunology
• Male
• Middle Aged
• Tuberculosis, Pulmonary/blood
• Tuberculosis, Pulmonary/immunology
• Young Adult