CD8+ T cells contribute to the development of transplant arteriosclerosis despite CD154 blockade.

CD8+ T cells contribute to the development of transplant arteriosclerosis despite CD154 blockade.

BACKGROUND: The CD40-CD154 receptor-ligand pair plays a critical role in allograft rejection by mediating the activation of endothelial cells, antigen-presenting cells, and T cells. Blockade of this interaction prevents acute allograft rejection and leads to prolonged allograft survival in numerous...

وصف كامل

التفاصيل البيبلوغرافية
المؤلفون الرئيسيون:	Ensminger, S, Witzke, O, Spriewald, B, Morrison, K, Morris, P, Rose, M, Wood, K
التنسيق:	Journal article
اللغة:	English
منشور في:	2000

مواد مشابهة

The persistence of transplant arteriosclerosis despite CD154 blockade.
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Intragraft interleukin-4 mRNA expression after short-term CD154 blockade may trigger delayed development of transplant arteriosclerosis in the absence of CD8+ T cells.
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Neutralizing interleukin-4 prevents transplant arteriosclerosis mediated by indirect pathway T cells under CD40-CD154 costimulation blockade.
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Critical role for IL-4 in the development of transplant arteriosclerosis in the absence of CD40-CD154 costimulation.
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Indirect allorecognition plays a pivotal role in the pathogenesis of transplant arteriosclerosis.
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Mouse endothelial CD40 expression does not play a role during the development of transplant arteriosclerosis.
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Kinetics of transplant arteriosclerosis in MHC-Class I mismatched and fully allogeneic mouse aortic allografts.
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Indirect allorecognition can play an important role in the development of transplant arteriosclerosis.
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Platelet-endothelial cell adhesion molecule-1 (CD31) expression on donor endothelial cells attenuates the development of transplant arteriosclerosis.
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Eosinophils are major effector cells for the development of transplant arteriosclerosis and depend on the presence of IL-4.
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Increased expression of transforming growth factor-beta and eosinophil infiltration is associated with the development of transplant arteriosclerosis in long-term surviving cardiac allografts.
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Regulation of transplant arteriosclerosis by CD25+CD4+ T cells generated to alloantigen in vivo.
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Development of a combined cardiac and aortic transplant model to investigate the development of transplant arteriosclerosis in the mouse.
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CD40-CD40 ligand-independent activation of CD8+ T cells can trigger allograft rejection.
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CD40-CD40L independent activation of CD8+T cells can trigger allograft rejection.
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Increased transplant arteriosclerosis in the absence of CCR7 is associated with reduced expression of Foxp3.
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Blockade of Cd40-Cd154 Interferes with Human T cell Engraftment in Scid Mice
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CD8+CD122+PD-1+ Tregs Synergize With Costimulatory Blockade of CD40/CD154, but Not B7/CD28, to Prolong Murine Allograft Survival
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CD40/CD154 blockade inhibits dendritic cell expression of inflammatory cytokines but not costimulatory molecules.
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CD4+ regulatory T cells generated in vitro with IFN-{gamma} and allogeneic APC inhibit transplant arteriosclerosis.
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Tumor necrosis factor-α blockade treatment decreased CD154 (CD40-ligand) expression in rheumatoid arthritis.
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Cutting edge: CD4+CD25+ alloantigen-specific immunoregulatory cells that can prevent CD8+ T cell-mediated graft rejection: implications for anti-CD154 immunotherapy.
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CD154 blockade alters innate immune cell recruitment and programs alloreactive CD8+ T cells into KLRG-1(high) short-lived effector T cells.
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Cutting edge: anti-CD154 therapeutic antibodies induce infectious transplantation tolerance.
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Dependency of direct pathway CD4+ T cells on CD40-CD154 costimulation is determined by nature and microenvironment of primary contact with alloantigen.
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The CD40-CD154 system in anti-infective host defense.
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Islet allograft rejection can be mediated by CD4+, alloantigen experienced, direct pathway T cells of TH1 and TH2 cytokine phenotype.
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CD 154: strong gluten wheat with high yield potential
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The Inhibition of CD40/CD154 Costimulatory Signaling in the Prevention of Renal Transplant Rejection in Nonhuman Primates: A Systematic Review and Meta Analysis
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