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Li K, Anderson KJ, Peng Q, et al. Cyclic AMP plays a critical role in C3a-receptor-mediated regulation of dendritic cells in antigen uptake and T cell stimulation. Blood 2008 [Epub ahead of print]. Authors found that engagement of C3a receptor (C3aR) on the surface of dendritic cells leads to alterations in the level of intracellular cAMP, a potent negative regulator of inflammatory responses. C3aR activation-induced depression of cAMP was associated with enhanced capacity of dendritic cells for antigen uptake and T-cell stimulation. The finding of a link between complement and adaptive immune stimulation through cAMP offers new insight into how innate and adaptive immunity combines to generate efficient effector and memory responses.
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Li, K.1
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This study demonstrated that locally produced C5a and C3a anaphylatoxins interacting with their G protein-coupled receptors (GPCRs), C5aR and C3aR, on APCs and T cells both upstream and downstream of CD28 and CD40L signalling are integrally involved in T-cell proliferation and differentiation. C5aR and C3aR mediated their effects through PI-3 kinase-gamma-dependent AKT phosphorylation, providing a link between GPCR signalling, CD28 costimulation and T-cell survival
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Strainic MG, Liu J, Huang D, et al. Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells. Immunity 2008; 28:425-435. This study demonstrated that locally produced C5a and C3a anaphylatoxins interacting with their G protein-coupled receptors (GPCRs), C5aR and C3aR, on APCs and T cells both upstream and downstream of CD28 and CD40L signalling are integrally involved in T-cell proliferation and differentiation. C5aR and C3aR mediated their effects through PI-3 kinase-gamma-dependent AKT phosphorylation, providing a link between GPCR signalling, CD28 costimulation and T-cell survival.
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Locally produced C5a binds to T cell-expressed C5aR to enhance effector T-cell expansion by limiting antigen-induced apoptosis
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+ T cells. Authors demonstrated that T-cell expansion induced by DAF-deficient APCs was augmented with diminished T-cell apoptosis, whereas T-cell expansion induced by C3-/- APCs was reduced because of enhanced T-cell apoptosis. These effects were traced to locally produced C5a, which through binding to T-cell-expressed C5aR, enhanced expression of Bcl-2 and prevented Fas upregulation. The results show that C5aR signal transduction in T cells is important to allow optimal T-cell expansion, as well as to maintain naive cell viability, and does so by suppressing programmed cell death
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+ T cells. Authors demonstrated that T-cell expansion induced by DAF-deficient APCs was augmented with diminished T-cell apoptosis, whereas T-cell expansion induced by C3-/- APCs was reduced because of enhanced T-cell apoptosis. These effects were traced to locally produced C5a, which through binding to T-cell-expressed C5aR, enhanced expression of Bcl-2 and prevented Fas upregulation. The results show that C5aR signal transduction in T cells is important to allow optimal T-cell expansion, as well as to maintain naive cell viability, and does so by suppressing programmed cell death.
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+ T lymphocytes isolated from the lectin pathway of patients undergoing bariatric surgery contain T cells that spontaneously secrete a cytokine pattern consistent with that from CD46-activated T cells. Authors suggest thatCD46-induced Tregs might play a role in intestinal immune homeostasis in which they could dampen unwanted effector T-cell responses
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+ T lymphocytes isolated from the lectin pathway of patients undergoing bariatric surgery contain T cells that spontaneously secrete a cytokine pattern consistent with that from CD46-activated T cells. Authors suggest thatCD46-induced Tregs might play a role in intestinal immune homeostasis in which they could dampen unwanted effector T-cell responses.
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Alford, S.K.1
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In this study, authors observed that mouse cardiac allograft rejection is accelerated in C1q-/- recipients compared with wild-type recipients, suggesting a protective role for C1q in the rejection process. Although the mechanisms by which C1q mediates the protective effects in allograft rejection are not clear, it seems not due to the alteration of allospecific T-cell response, instead the C1q may help recipient macrophages/dendritic cells to phagocytose apoptotic bodies within the graft to render the graft less inflammation
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Csencsits K, Burrell BE, Lu G, et al. The classical complement pathway in transplantation: unanticipated protective effects of C1q and role in inductive antibody therapy. Am J Transplant 2008; 8:1622-1630. In this study, authors observed that mouse cardiac allograft rejection is accelerated in C1q-/- recipients compared with wild-type recipients, suggesting a protective role for C1q in the rejection process. Although the mechanisms by which C1q mediates the protective effects in allograft rejection are not clear, it seems not due to the alteration of allospecific T-cell response, instead the C1q may help recipient macrophages/dendritic cells to phagocytose apoptotic bodies within the graft to render the graft less inflammation.
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