scholarly journals Transforming growth factor-β controls T helper type 1 cell development through regulation of natural killer cell interferon-γ

2005 ◽  
Vol 6 (6) ◽  
pp. 600-607 ◽  
Author(s):  
Yasmina Laouar ◽  
Fayyaz S Sutterwala ◽  
Leonid Gorelik ◽  
Richard A Flavell
Keyword(s):  
Growth Factor ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Transforming Growth Factor ◽  
Killer Cell ◽  
Transforming Growth Factor Β ◽  
Interferon Γ ◽  
T Helper ◽  
Helper Type

scholarly journals Transforming Growth Factor-β-activated Kinase 1 Regulates Natural Killer Cell-mediated Cytotoxicity and Cytokine Production

2011 ◽  
Vol 286 (36) ◽  
pp. 31213-31224 ◽  
Author(s):  
Kamalakannan Rajasekaran ◽  
Haiyan Chu ◽  
Pawan Kumar ◽  
Yechen Xiao ◽  
Mathew Tinguely ◽  
...  
Keyword(s):  
Growth Factor ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Cytokine Production ◽  
Transforming Growth Factor ◽  
Killer Cell ◽  
Transforming Growth Factor Β

scholarly journals 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.

1996 ◽  
Vol 183 (6) ◽  
pp. 2669-2674 ◽  
Author(s):  
F Powrie ◽  
J Carlino ◽  
M W Leach ◽  
S Mauze ◽  
R L Coffman
Keyword(s):  
T Cells ◽  
Growth Factor ◽  
Cd4 T Cells ◽  
Transforming Growth Factor ◽  
Th2 Cells ◽  
Tgf Beta ◽  
T Helper ◽  
Cd4 Cells ◽  
Helper Type

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

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