Articles: regulatory-t-lymphocytes.
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Allogeneic liver transplantation induces spontaneous tolerance in mice without a requirement for immunosuppression. The underling mechanisms remain unclear. Our recent studies indicated that Foxp3(+)CD25(+)CD4(+) regulatory T (Treg) cells play an important role in the induction of spontaneous transplant tolerance. ⋯ Immunohistochemistry revealed reduced Foxp3(+) cells and significantly increased IL-2, IL-10, and IFN-γ producing elements in the liver grafts and recipient spleens of Flt3L-/- and PD-L1-/- donors. In conclusion, liver DCs play a critical role in the induction of Foxp3(+)CD25(+)CD4(+) Treg, which may mediate spontaneous acceptance of MHC-mismatched liver allografts in mice. The effects of DCs on Foxp3(+)CD25(+)CD4(+) Treg induction and expansion appear to depend on the PD-L1 signal.
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Int. Immunopharmacol. · May 2013
The imbalance of Th17/Treg in Chinese children with Henoch-Schonlein purpura.
Interleukin 17 (IL-17)-producing T helper (Th17) cells and CD4(+)CD25(+) regulatory T (Treg) cells are two new T-cell subsets that are thought to be critically involved in mediating and regulating autoimmune responses. The imbalance of Th17/Treg cells has been implicated in a wide range of autoimmune disorders. The aim of our study was to determine whether the Th17/Treg balance was abnormal in children with Henoch-Schonlein Purpura (HSP). ⋯ The Th17/Treg ratio was positively correlated with the erythrocyte sedimentation rate (ESR), kidney lesions and the clinical symptom of the presence of more than two organ systems with lesions. However, the ratio had no correlation with anti-streptolysin O (ASO) or complement 3 (C3) levels. These results indicate that a Th17/Treg imbalance exists in HSP, and it appears to be closely related to the disease onset.
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The extent to which T-cell-mediated immune surveillance is impaired in human cancer remains a question of major importance, given its potential impact on the development of generalized treatments of advanced disease where the highest degree of heterogeneity exists. Here, we report the first global analysis of immune dysfunction in patients with advanced hepatocellular carcinoma (HCC). Using multi-parameter fluorescence-activated cell sorting analysis, we quantified the cumulative frequency of regulatory T cells (Treg), exhausted CD4(+) helper T cells, and myeloid-derived suppressor cells (MDSC) to gain concurrent views on the overall level of immune dysfunction in these inoperable patients. ⋯ In dampening T-cell-mediated antitumor immunity, we hypothesized that these processes may facilitate HCC progression and thwart the efficacy of immunotherapeutic interventions. In testing this hypothesis, we showed that combined regimens to deplete Tregs, MDSC, and PD-1(+) T cells in patients with advanced HCC restored production of granzyme B by CD8(+) T cells, reaching levels observed in normal controls and also modestly increased the number of IFN-γ producing CD4(+) T cells. These clinical findings encourage efforts to restore T-cell function in patients with advanced stage disease by highlighting combined approaches to deplete endogenous suppressor cell populations that can also expand effector T-cell populations.
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The fine balance of Th17/Treg is crucial for maintenance of immune homeostasis. The objective of this study was to investigate the balance of Th17/Treg and the expression of related cytokines in Uighur cervical cancer patients. ⋯ The virtual slide for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1813823795931511.
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Asthma is a common inflammatory disease involving cross-talk between innate and adaptive immunity. We reveal that antibacterial innate immunity protein, peptidoglycan recognition protein (Pglyrp)1, is involved in the development of allergic asthma. Pglyrp1(-/-) mice developed less severe asthma than wild-type (WT) mice following sensitization with house dust mite (allergen) (HDM). ⋯ In vivo depletion of pDC in HDM-sensitized Pglyrp1(-/-) mice reversed the low responsive asthma phenotype of Pglyrp1(-/-) mice to resemble the more severe WT phenotype. Thus, Pglyrp1(-/-) mice efficiently control allergic asthma by upregulating pDC and Treg cells in the lungs, whereas in WT mice, Pglyrp1 is proinflammatory and decreases pDC and Treg cells and increases proasthmatic Th2 and Th17 responses. Blocking Pglyrp1 or enhancing pDC in the lungs may be beneficial for prevention and treatment of asthma.