Neutralizing interleukin-4 prevents transplant arteriosclerosis mediated by indirect pathway T cells under CD40-CD154 costimulation blockade.

Neutralizing interleukin-4 prevents transplant arteriosclerosis mediated by indirect pathway T cells under CD40-CD154 costimulation blockade.

INTRODUCTION: Blockade of the CD40-CD154 costimulatory pathway can prolong allograft survival, but does not prevent the development of transplant arteriosclerosis in several models. In this study, we investigated the mechanisms of CD40-CD154-independent transplant arteriosclerosis in major histocom...

תיאור מלא

מידע ביבליוגרפי
Main Authors:	Spriewald, B, Ensminger, S, Bushell, A, Wood, K
פורמט:	Journal article
שפה:	English
יצא לאור:	2008

פריטים דומים

Critical role for IL-4 in the development of transplant arteriosclerosis in the absence of CD40-CD154 costimulation.
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CD8+ T cells contribute to the development of transplant arteriosclerosis despite CD154 blockade.
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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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Mouse endothelial CD40 expression does not play a role during the development of transplant arteriosclerosis.
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Indirect allorecognition plays a pivotal role in the pathogenesis of transplant arteriosclerosis.
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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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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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