Investigation on antigen-specific T cell responses in type 2 diabetes mellitus patients / 中华内分泌代谢杂志

Objective To investigate the antigen-specific T cell functionality in type 2 diabetes mellitus patients. Methods Peripheral blood from 38 type 2 diabetes mellitus patients and 47 health controls (control group) have been collected. The proportions of CD4+and CD8+T cell as well as the ratio of CD4+/CD8+were monitored by flow cytometry. Meanwhile, antigen- nonspecific and specific Th1 responses were compared between two groups through detecting interferon (IFN)-γ, interleukin 2 (IL-2), and tumor necrosis factor (TNF)-α producing cells upon propylene glycol monomethyl ether acetate (PMA)/ionomycine and epstein-barr virus ( EBV) peptides stimulation, respectively followed by an intracellular cytokine staining. Results Compared to control group, the proportion of CD4+T cell and the ratio of CD4+/CD8+were significantly increased in type 2 diabetes mellitus group (P＜0.05) whereas CD8+T cells exhibited no significant difference between two groups. Antigen-nonspecific Th1 responses in type 2 diabetes mellitus patients were significantly decreased, demonstrated by lower percentages of IFN-γ, IL-2, and TNF-α producing CD4+T cells when compared to control group , while CD8+T cells in type 2 diabetes mellitus patients exhibited similar cytokine production patterns. However, when stimulated by EBV specific peptides, the percentages of IFN-γ, IL-2, and TNF-α producing CD8+T cells were significantly higher in type 2 diabetes mellitus patients than those in control group (P＜0.05). HbA1Cwas positively correlated with the percentage of EBV-specific TNF-α producing CD8+T cells (P＜0.05). Conclusion In type 2 diabetes mellitus, the secretion capacity of CD4+and CD8+T cell was significantly decreased and the antigen-specific responses represent the presence of an abnormal activated status, which indicates that chronic hyperglycemia may damage T cells function and aggravate chronic inflammation.

Immune responses to mycobacterial antigens in sarcoidosis: A systematic review.

From the time sarcoidosis has been described, there has always been a viewpoint that the disease is in some way related to tuberculosis (TB). Sarcoidosis is a granulomatous disease, which is likely a result of continued presentation of a poorly degradable antigen. Mycobacterium tuberculosis has been a very strong contender for this antigen. Besides the molecular studies demonstrating mycobacterial deoxyribonucleic acid (DNA) in the sarcoid tissue, assessment of immune responses against mycobacterial antigens provides a useful tool to study the role of mycobacteria in the pathogenesis of sarcoidosis. We reviewed the studies focussing on T-cell and B-cell responses to tubercular antigens in patients with sarcoidosis. Pooled data from various studies does provide a suggestive, though not unequivocal evidence in favour of mycobacteria as a cause of sarcoidosis. These findings not only reinforce the possible pathogenic role of mycobacterial antigens in sarcoidosis, but at the same time also limit the clinical utility of molecular and serological studies based on mycobacterial antigens in the differential diagnosis of TB from sarcoidosis, particularly in a country with high endemicity for TB.

Impairment of cytomegalovirus-specific cellular immune response as a risk factor for cytomegalovirus disease in transplant recipients: [review]

Human cytomegalovirus (CMV) infection is common in most people but nearly asymptomatic in immunocompetent individuals. After primary infection the virus persists throughout life in a latent form in a variety of tissues, particularly in precursor cells of the monocytic lineage. CMV reinfection and occurrence of disease are associated with immunosuppressive conditions. Solid organ and bone marrow transplant patients are at high risk for CMV disease as they undergo immunosuppression. Antiviral treatment is effective in controlling viremia, but 10-15 percent of infected patients can experience CMV disease by the time the drug is withdrawn. In addition, long-term antiviral treatment leads to bone marrow ablation and renal toxicity. Furthermore, control of chronic CMV infection in transplant recipients appears to be dependent on the proper recovery of cellular immunity. Recent advances in the characterization of T-cell functions and identification of distinct functional signatures of T-cell viral responses have opened new perspectives for monitoring transplant individuals at risk of developing CMV disease.