A critical role for transforming growth factor-beta but not interleukin 4 in the suppression of T helper type 1-mediated colitis by CD45RB(low) CD4+ T cells.

T helper cell
DOI: 10.1084/jem.183.6.2669 Publication Date: 2004-06-24T07:56:10Z
ABSTRACT
A T helper type 1 (Th1)-mediated colitis with similarities to inflammatory bowel disease in humans developed severe combined immunodeficiency mice reconstituted CD45RB(high) CD4+ splenic cells and could be prevented by cotransfer of CD45RB(low) cells. Inhibition this Th1 response the cell population reversed vivo an anti-transforming growth factor (TGF) beta antibody. Interleukin (IL) 4 was not required for either differentiation function protective as from IL-4-deficient were fully effective. These results identify a subpopulation peripheral TGF-beta critical components natural immune regulatory mechanism, which prevents development pathogenic responses gut, suggests that immunoregulatory is distinct Th2
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