Sustained exposure to bacterial antigen induces interferon-γ-dependent T cell receptor ζ down-regulation and impaired T cell function

10.1038/ni975 ◽  
2003 ◽  
Vol 4 (10) ◽  
pp. 957-964 ◽  
Author(s):  
Noemí Bronstein-Sitton ◽  
Leonor Cohen-Daniel ◽  
Ilan Vaknin ◽  
Analía V Ezernitchi ◽  
Benny Leshem ◽  
...  
2012 ◽  
Vol 109 (5) ◽  
pp. 1625-1630 ◽  
Author(s):  
A. Zanin-Zhorov ◽  
J. Lin ◽  
J. Scher ◽  
S. Kumari ◽  
D. Blair ◽  
...  

Surgery ◽  
2001 ◽  
Vol 129 (6) ◽  
pp. 749-756 ◽  
Author(s):  
Diane C. Lockhart ◽  
Allen K. Chan ◽  
Simona Mak ◽  
Hong-Gu Joo ◽  
Heather A. Daust ◽  
...  

Cell ◽  
1989 ◽  
Vol 57 (3) ◽  
pp. 483-492 ◽  
Author(s):  
David A. Ferrick ◽  
Suryaprakash R. Sambhara ◽  
Wolfgang Ballhausen ◽  
Aikichi Iwamoto ◽  
Hanspeter Pircher ◽  
...  

2015 ◽  
Vol 396 (5) ◽  
pp. 555-569 ◽  
Author(s):  
Luca Simeoni ◽  
Ivan Bogeski

Abstract T-cell receptor (TCR) triggering by antigens activates a sophisticated intracellular signaling network leading to transcriptional activation, proliferation and differentiation of T cells. These events ultimately culminate in adaptive immune responses. Over recent years it has become evident that reactive oxygen species (ROS) play an important role in T-cell activation. It is now clear that ROS are involved in the regulation of T-cell mediated physiological and pathological processes. Upon TCR triggering, T cells produce oxidants, which originate from different cellular sources. In addition, within inflamed tissues, T cells are exposed to exocrine ROS produced by activated phagocytes or other ROS-producing cells. Oxidative modifications can have different effects on T-cell function. Indeed, they can stimulate T-cell activation but they can be also detrimental. These opposite effects of oxidation likely depend on different factors such as ROS concentration and source and also on the differentiation status of the T cells. Despite the well-stablished fact that ROS represent important modulators of T-cell activation, the precise molecular mechanisms of their action are far from clear. Here, we summarize the present knowledge on redox regulation of T-cell function with a particular emphasis on the redox regulation of TCR signaling.


Blood ◽  
2009 ◽  
Vol 113 (10) ◽  
pp. 2229-2237 ◽  
Author(s):  
Ludmila Jirmanova ◽  
Dandapantula N. Sarma ◽  
Dragana Jankovic ◽  
Paul R. Mittelstadt ◽  
Jonathan D. Ashwell

AbstractT cells possess a p38 activation alternative pathway in which stimulation via the antigen receptor (T-cell receptor [TCR]) induces phosphorylation of p38α and β on Tyr323. To assess the contribution of this pathway to normal T-cell function, we generated p38α knockin mice in which Tyr323 was replaced with Phe (p38αY323F). TCR-mediated stimulation failed to activate p38αY323F as measured by phosphorylation of the Thr-Glu-Tyr activation motif and p38α catalytic activity. Cell-cycle entry was delayed in TCR-stimulated p38αY323F T cells, which also produced less interferon (IFN)–γ than wild-type T cells in response to TCR-mediated but not TCR-independent stimuli. p38αY323F mice immunized with T-helper 1 (Th1)–inducing antigens generated normal Th1 effector cells, but these cells produced less IFN-γ than wild-type cells when stimulated through the TCR. Thus, the Tyr323-dependent pathway and not the classic mitogen-activated protein (MAP) kinase cascade is the physiologic means of p38α activation through the TCR and is necessary for normal Th1 function but not Th1 generation.


Immunity ◽  
2010 ◽  
Vol 32 (5) ◽  
pp. 670-680 ◽  
Author(s):  
Roza I. Nurieva ◽  
Shuling Zheng ◽  
Wei Jin ◽  
Yeonseok Chung ◽  
Yongliang Zhang ◽  
...  

2017 ◽  
Vol 216 (9) ◽  
pp. 1164-1175 ◽  
Author(s):  
James H McLinden ◽  
Nirjal Bhattarai ◽  
Jack T Stapleton ◽  
Qing Chang ◽  
Thomas M Kaufman ◽  
...  

2021 ◽  
Vol 27 (3) ◽  
pp. S6-S7
Author(s):  
Daniel Peltier ◽  
Sethuramasundaram Pitchiaya ◽  
Visweswaran Ravikumar ◽  
Thomas Decoville ◽  
Sherri Wood ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document