T cell receptor specific apoptosis: an endogenous mechanism for T cell homeostasis and potential strategy for antigen modulation of disease

APOPTOSIS ◽  
1996 ◽  
Vol 1 (4) ◽  
pp. 247-251 ◽  
Author(s):  
J. M. Critchfield



2004 ◽  
Vol 65 (9-10) ◽  
pp. S26
Author(s):  
Stephanie Le Bas-Bernadet ◽  
Anne Hutchings ◽  
Clement Asiedu ◽  
Judith M. Thomas


2012 ◽  
Vol 425 (1) ◽  
pp. 107-112 ◽  
Author(s):  
Keiko Doi ◽  
Takahiro Fujimoto ◽  
Tadashi Okamura ◽  
Masahiro Ogawa ◽  
Yoko Tanaka ◽  
...  


Immunity ◽  
2011 ◽  
Vol 35 (3) ◽  
pp. 349-360 ◽  
Author(s):  
Kyla Omilusik ◽  
John J. Priatel ◽  
Xiaoxi Chen ◽  
Yiwen Teresa Wang ◽  
Hongjian Xu ◽  
...  


Immunity ◽  
2010 ◽  
Vol 32 (2) ◽  
pp. 214-226 ◽  
Author(s):  
Jae-Ho Cho ◽  
Hee-Ok Kim ◽  
Charles D. Surh ◽  
Jonathan Sprent


2018 ◽  
Vol 218 (suppl_5) ◽  
pp. S508-S518 ◽  
Author(s):  
Emily Speranza ◽  
Paula Ruibal ◽  
Julia R Port ◽  
Feng Feng ◽  
Lia Burkhardt ◽  
...  

Abstract Differences in T-cell phenotype, particularly the expression of markers of T-cell homeostasis, have been observed in fatal and nonfatal Ebola virus disease (EVD). However, the relationship between these markers with T-cell function and virus clearance during EVD is poorly understood. To gain biological insight into the role of T cells during EVD, combined transcriptomics and T-cell receptor sequencing was used to profile blood samples from fatal and nonfatal EVD patients from the recent West African EVD epidemic. Fatal EVD was characterized by strong T-cell activation and increased abundance of T-cell inhibitory molecules. However, the early T-cell response was oligoclonal and did not result in viral clearance. In contrast, survivors mounted highly diverse T-cell responses, maintained low levels of T-cell inhibitors, and cleared Ebola virus. Our findings highlight the importance of T-cell immunity in surviving EVD and strengthen the foundation for further research on targeting of the dendritic cell-T cell interface for postexposure immunotherapy.



2009 ◽  
Vol 29 (10) ◽  
pp. 2594-2608 ◽  
Author(s):  
Tamara Copetti ◽  
Cosetta Bertoli ◽  
Emiliano Dalla ◽  
Francesca Demarchi ◽  
Claudio Schneider

ABSTRACT Recently, autophagy has emerged as a critical process in the control of T-cell homeostasis. Given the pivotal role of NF-κB in the signaling events of T cells, we have analyzed and unveiled a conserved NF-κB binding site in the promoter of the murine and human BECN1 autophagic gene (Atg6). Accordingly, we demonstrate that the NF-κB family member p65/RelA upregulates BECN1 mRNA and protein levels in different cellular systems. Moreover, p65-mediated upregulation of BECN1 is coupled to increased autophagy. The newly identified κB site in the BECN1 promoter specifically interacts with p65 both in vitro and in living Jurkat cells upon phorbol myristate acetate (PMA)-ionomycin stimulation, where p65 induction is coupled to BECN1 upregulation and autophagy induction. Finally, anti-CD3- and PMA-ionomycin-mediated activation of T-cell receptor signaling in peripheral T cells from lymph nodes of healthy mice results in an upregulation of BECN1 expression that can be blocked by the NF-κB inhibitor BAY 11-7082. Altogether, these data suggest that autophagy could represent a novel route modulated by p65 to regulate cell survival and control T-cell homeostasis.



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