نتایج جستجو برای: cd8 t cell anergy

تعداد نتایج: 2174751  

Journal: :Immunity 2008
Irene Puga Anjana Rao Fernando Macian

T cell receptor (TCR) engagement in the absence of costimulation induces the calcium-dependent upregulation of a program of gene expression that leads to the establishment of T cell anergy. Casp3 is one of the genes activated during anergy induction. Here we show that caspase 3 is required for the induction of T cell unresponsiveness. Suboptimal T cell stimulation induced caspase 3 activation, ...

2014
Antoine Marcais Rory Blevins Johannes Graumann Amelie Feytout Gopuraja Dharmalingam Thomas Carroll Inês F. Amado Ludovica Bruno Keunwook Lee Thierry Walzer Matthias Mann Antonio A. Freitas Mark Boothby Amanda G. Fisher Matthias Merkenschlager

T cell receptor (TCR) signals can elicit full activation with acquisition of effector functions or a state of anergy. Here, we ask whether microRNAs affect the interpretation of TCR signaling. We find that Dicer-deficient CD4 T cells fail to correctly discriminate between activating and anergy-inducing stimuli and produce IL-2 in the absence of co-stimulation. Excess IL-2 production by Dicer-de...

Journal: :EMBO reports 2008
Yan Zheng Yuanyuan Zha Thomas F Gajewski

The activation of T cells is tightly controlled by many positive and negative regulatory processes. This fine-tuning allows productive immunity to pathogens while minimizing the risk of autoimmunity. One negative regulatory mechanism is clonal anergy, which is a hyporesponsive state that occurs when T cells are activated through the T-cell antigen receptor in the absence of appropriate co-stimu...

Journal: :Infection and immunity 1997
A Brás L Rodríguez-Borlado A González-Garcia C Martínez-A

Increased interest has recently been focused on nitric oxide (NO) due to its several biological roles. Apart from being a potential antimicrobial defense and a mediator of autoimmune diseases, NO also appears to be a strong mediator of T-cell responses. In this report, we have characterized the effect of NO on T-cell function. For this purpose, we analyzed in vivo T-cell responses to the bacter...

Journal: :The Journal of Experimental Medicine 1994
J Sloan-Lancaster B D Evavold P M Allen

We have demonstrated Th2 clonal anergy as a consequence of partial T cell activation by immunogenic peptide and chemically fixed APC, as well as by altered peptide ligand and live antigen-presenting cells (APC). Either stimulation resulted in a profound inability of the T cells to proliferate upon restimulation with antigen and functional APC, a similar phenomenon to that found with Th1 cells. ...

Journal: :Journal of immunology 2004
Shahin Ranjbar Nary Ly Sok Thim Jean-Marc Reynes Anne E Goldfeld

Mycobacterium tuberculosis (MTb) is the leading cause of death in the setting of AIDS. MTb enhances the pathogenicity and accelerates the course of HIV disease and, furthermore, infection with HIV-1 increases the risk of reactivation or reinfection with MTb. In this study, we show that host-specific recall responses to one pathogen, MTb, has a direct effect upon the regulation of a second patho...

Journal: :Journal of virology 2000
L Bouhdoud P Villain A Merzouki M Arella C Couture

Human immunodeficiency virus type 1 (HIV-1) infection triggers a cytotoxic T-lymphocyte (CTL) response mediated by CD8(+) and perhaps CD4(+) CTLs. The mechanisms by which HIV-1 escapes from this CTL response are only beginning to be understood. However, it is already clear that the extreme genetic variability of the virus is a major contributing factor. Because of the well-known ability of alte...

Journal: :Blood 2002
David Spaner Xiaofang Sheng-Tanner Andre C Schuh

Acute graft-versus-host disease (GVHD) after allogeneic stem cell transplantation is associated with impaired deletion and anergy of host-reactive T cells. To elucidate the immunoregulatory events that may contribute to such dysregulated T-cell responses in GVHD, we studied superantigen (SAg) responses after adoptive T-cell transfer into severe combined immunodeficient (SCID) mice. SAg response...

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