(C) 2011 Elsevier B V All rights reserved “
“P>Uncommitt

(C) 2011 Elsevier B.V. All rights reserved.”
“P>Uncommitted (naive) CD4+ T helper cells (Thp) can be induced to differentiate to specific lineages according

to the local cytokine milieu, towards T helper type 1 (Th1), Th2, Th17 and regulatory T cell (T(reg)) phenotypes in a mutually exclusive manner. Each phenotype is characterized by unique signalling pathways and expression of specific transcription factors, notably T-bet for Th1, GATA-3 for Th2, forkhead box P3 (FoxP3) for T(regs) and receptor-related orphan receptor (ROR)alpha and ROR gamma t for Th17 cells. T(regs) and Th17 cells have been demonstrated to arise from common precursors in a reciprocal manner based on exposure to transforming growth factor (TGF)-beta or TGF-beta plus interleukin (IL)-6 and carry out diametrically opposing functions, namely suppression or propagation of inflammation, respectively. buy SCH 900776 However, while epigenetic modifications in Th1 and Th2 differentiated cells prevents their conversion to other phenotypes, Th17 cells generated in vitro using TGF-beta and IL-6 are unstable and can convert to other

phenotypes, especially Th1, both in vitro and in vivo. T(regs) are generated from naive precursors both in the thymus (natural, nT(regs)) and in the periphery (induced, iT(regs)). The highly suppressive function of T(regs) enables them to control many inflammatory diseases in animals and makes them particularly buy STI571 attractive candidates for immunotherapy in humans. The stability of the T(reg) phenotype is therefore of paramount importance

in this context. Recent descriptions of T(reg) biology have suggested that components of pathogens or inflammatory mediators may subvert the suppressive function of T(regs) in order to allow propagation of adequate immune responses. Unexpectedly, however, a number of groups have now described conversion of T(regs) to the Th17 phenotype induced by appropriate Syk inhibitor inflammatory stimuli. These observations are particularly relevant in the context of cell therapy but may also explain some of the dysregulation seen in autoimmune diseases. In this paper, we review T(reg) to Th17 conversion and propose some potential mechanisms for this phenomenon.”
“The sulphur and nitrogen mustards are strong alkylating agents, which induces inflammations of the skin including blistering right up to ulcerations. Depending on the severity, the wounds may need weeks to heal. In the past it was shown that sulphur mustard has a destructive effect on endothelial precursor cells, which have been shown to play a pivotal role in the wound healing reaction by inducing neovascularisation. However, for these alkylating agents as well as for sulphur mustard nothing is known about their effects on endothelial precursors.

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