Effector CD4+ T cells, the cytokines they generate, and GVHD: something old and something new

JM Coghill, S Sarantopoulos, TP Moran… - Blood, The Journal …, 2011 - ashpublications.org
JM Coghill, S Sarantopoulos, TP Moran, WJ Murphy, BR Blazar, JS Serody
Blood, The Journal of the American Society of Hematology, 2011ashpublications.org
GVHD is a syndrome that results from minor and major histocompatibility complex
incompatibilities between the donor and recipient. More than 50 years after its initial
description, the pathophysiology of GVHD remains poorly understood. Nonetheless, donor T
cells have been shown to be critical to the pathophysiology of acute and chronic GVHD, yet
precisely how they function remains unclear. The effector mechanisms by which donor T
cells mediate tissue inflammation is even less well understood. Identification of several new …
Abstract
GVHD is a syndrome that results from minor and major histocompatibility complex incompatibilities between the donor and recipient. More than 50 years after its initial description, the pathophysiology of GVHD remains poorly understood. Nonetheless, donor T cells have been shown to be critical to the pathophysiology of acute and chronic GVHD, yet precisely how they function remains unclear. The effector mechanisms by which donor T cells mediate tissue inflammation is even less well understood. Identification of several new lineages of CD4+ T cells made in the past decade and their roles in the pathophysiology of T cell–mediated diseases has shed new light on these effector mechanisms. In this review, we summarize the recent descriptions of these T-cell lineages and the current data supporting their role in acute and to a lesser extent chronic GVHD. Investigations into the activity of these new T-cell lineages may provide more rationale approaches to the treatment or prevention of GVHD.
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