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.

scholarly journals T Helper Type 2 Cell Differentiation Occurs in the Presence of Interleukin 12 Receptor β2 Chain Expression and Signaling

2000 ◽  
Vol 191 (5) ◽  
pp. 847-858 ◽  
Author(s):  
Ryuta Nishikomori ◽  
Rolf O. Ehrhardt ◽  
Warren Strober
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Th2 Cells ◽  
Interleukin 12 ◽  
Th1 Cells ◽  
T Helper ◽  
Ifn Γ ◽  
Helper Type

The differentiation of CD4+ T cells into T helper type 1 (Th1) cells is driven by interleukin (IL)-12 through the IL-12 receptor β2 (IL-12Rβ2) chain, whereas differentiation into Th2 cells is driven by IL-4, which downregulates IL-12Rβ2 chain. We reexamined such differentiation using IL-12Rβ2 chain transgenic mice. We found that CD4+ T cells from such mice were able to differentiate into Th2 cells when primed with IL-4 or IL-4 plus IL-12. In the latter case, the presence of IL-4 suppressed interferon (IFN)-γ production 10–100-fold compared with cells cultured in IL-12 alone. Finally, in studies of the ability of IL-12 to convert Th2 cells bearing a competent IL-12R to the Th1 cells, we showed that: (a) T cells bearing the IL-12Rβ2 chain transgene and primed under Th2 conditions could not be converted to Th1 cells by repeated restimulation under Th1 conditions; and (b) established Th2 clones transfected with the IL-12Rβ2 chain construct continued to produce IL-4 when cultured with IL-12. These studies show that IL-4–driven Th2 differentiation can occur in the presence of persistent IL-12 signaling and that IL-4 inhibits IFN-γ production under these circumstances. They also show that established Th2 cells cannot be converted to Th1 cells via IL-12 signaling.

scholarly journals Gfi1, a transcriptional repressor, inhibits the induction of the T helper type 1 programme in activated CD4 T cells

Immunology ◽  
2016 ◽  
Vol 147 (4) ◽  
pp. 476-487 ◽  
Author(s):  
Junpei Suzuki ◽  
Saho Maruyama ◽  
Hidekazu Tamauchi ◽  
Makoto Kuwahara ◽  
Mika Horiuchi ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Transcriptional Repressor ◽  
T Helper ◽  
Helper Type

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 Dectin-1 diversifies Aspergillus fumigatus–specific T cell responses by inhibiting T helper type 1 CD4 T cell differentiation

2011 ◽  
Vol 208 (2) ◽  
pp. 369-381 ◽  
Author(s):  
Amariliz Rivera ◽  
Tobias M. Hohl ◽  
Nichole Collins ◽  
Ingrid Leiner ◽  
Alena Gallegos ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
T Helper ◽  
Cell Responses ◽  
Ifn Γ ◽  
Th17 Differentiation ◽  
Helper Type

Pulmonary infection of mice with Aspergillus fumigatus induces concurrent T helper type 1 (Th1) and Th17 responses that depend on Toll-like receptor/MyD88 and Dectin-1, respectively. However, the mechanisms balancing Th1 and Th17 CD4 T cell populations during infection remain incompletely defined. In this study, we show that Dectin-1 deficiency disproportionally increases Th1 responses and decreases Th17 differentiation after A. fumigatus infection. Dectin-1 signaling in A. fumigatus–infected wild-type mice reduces IFN-γ and IL-12p40 expression in the lung, thereby decreasing T-bet expression in responding CD4 T cells and enhancing Th17 responses. Absence of IFN-γ or IL-12p35 in infected mice or T-bet in responding CD4 T cells enhances Th17 differentiation, independent of Dectin-1 expression, in A. fumigatus–infected mice. Transient deletion of monocyte-derived dendritic cells also reduces Th1 and boosts Th17 differentiation of A. fumigatus–specific CD4 T cells. Our findings indicate that Dectin-1–mediated signals alter CD4 T cell responses to fungal infection by decreasing the production of IL-12 and IFN-γ in innate cells, thereby decreasing T-bet expression in A. fumigatus–specific CD4 T cells and enabling Th17 differentiation.

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