Articles: regulatory-t-lymphocytes.
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The roles of regulatory T cells (Tregs) and PD-1 in hepatitis B have not been clearly described. Also, the role of B and T lymphocyte attenuator (BTLA), which serves as a negative regulator of T-cell activation, is still unknown in hepatitis B. In this study, we analyzed the frequency of circulating CD4(+)CD25(high) Tregs in patients with chronic hepatitis B (CHB), and subsequently investigated expression of PD-1 and BTLA on CD4(+) T cells, as well as their relationships with the clinical index of CHB patients. ⋯ The frequency of Tregs was significantly higher in patients with HBV DNA titers >or=10(8) than in those with HBV DNA titers <10(8). Circulating CD4(+)CD25(high) Treg frequency and PD-1 expression on CD4(+) T cells correlated positively with serum HBV DNA load in CHB patients. Our findings suggest that the increased frequency of CD4(+)CD25(high) Tregs and PD-1 expression on CD4(+) T lymphocytes may inhibit the cellular immune response against HBV and affect viral clearance, leading to the persistence of chronic HBV infection.
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Adverse cardiovascular events resulting from accelerated atherosclerosis are the leading cause of mortality in uraemic patients on maintenance haemodialysis (MHD). Chronic inflammation due to antigen-specific responses is an important factor in the acceleration of atherosclerosis. The balance between CD4(+) CD25(+) forkhead/winged helix transcription factor (Foxp3)(+) regulatory T cells (Treg) and T helper (Th)17 cells has been reported to play an important role in the development of inflammatory and autoimmune diseases. The aim of the present study was to assess the Treg/Th17 pattern in uraemic patients on MHD and to explore the significance of Treg/Th17 imbalance in the development and outcome of acute cardiovascular events. ⋯ The Treg/Th17 balance was disturbed by uraemia, especially in patients with adverse cardiovascular events. This Th17/Treg imbalance might act synergistically with microinflammation on immune-mediated atherosclerosis and contribute to the high incidence of adverse cardiovascular events.
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Regulatory/suppressor T cells (Tregs) maintain immunologic homeostasis and prevent autoimmunity. They are the guardians of dominant tolerance. Recent research reveals quantitative and/or functional defect of Tregs in systemic autoimmune diseases. ⋯ Immunosuppressive treatments, like corticosteroids and anti-TNF, modulate Tregs cells population. There is increasing interest in the use of Tregs as a biological therapy to preserve and restore tolerance to self-antigen. However, difficulties to characterize these lymphocytes and controversies in the results of studies refrain their use in current clinical practice.
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Obstructive nephropathy is characterized by an inflammatory state in the kidney, that is promoted by cytokines and growth factors produced by damaged tubular cells, infiltrated macrophages and accumulated myofibroblasts. This inflammatory state contributes to tubular atrophy and interstitial fibrosis characteristic of obstructive nephropathy. ⋯ Increased angiotensin II production, increased oxidative stress and high levels of proinflammatory cytokines contribute to NF-kappaB activation which in turn induce the expression of adhesion molecules and chemokines responsible for leukocyte recruitment and iNOS and cytokines overexpression, which aggravates the inflammatory response in the damaged kidney. In this manuscript we revise the different events and regulatory mechanisms involved in inflammation associated to obstructive nephropathy.