Selective engraftment of memory CD4+ T cells with an unusual recirculation pattern and a diverse T cell receptor-Vβ repertoire into scid mice

1993 ◽  
Vol 23 (2) ◽  
pp. 350-356 ◽  
Author(s):  
Jörg Reimann ◽  
Angelika Rudoiphi ◽  
Thomas Tscherning ◽  
Mogens H. Claesson
Immunity ◽  
1995 ◽  
Vol 2 (2) ◽  
pp. 177-184 ◽  
Author(s):  
Randle Ware ◽  
Hong Jiang ◽  
Ned Braunstein ◽  
Jennifer Kent ◽  
Ethan Wiener ◽  
...  

2001 ◽  
Vol 194 (6) ◽  
pp. 719-732 ◽  
Author(s):  
Saied Mirshahidi ◽  
Ching-Tai Huang ◽  
Scheherazade Sadegh-Nasseri

Induction of tolerance in self-reactive memory T cells is an important process in the prevention of autoimmune responses against peripheral self-antigens in autoimmune diseases. Although naive T cells can readily be tolerized, memory T cells are less susceptible to tolerance induction. Recently, we demonstrated that low avidity engagement of T cell receptor (TCR) by low densities of agonist peptides induced anergy in T cell clones. Since memory T cells are more responsive to lower antigenic stimulation, we hypothesized that a low avidity TCR engagement may induce tolerance in memory T cells. We have explored two antigenic systems in two transgenic mouse models, and have tracked specific T cells that are primed and show memory phenotype. We demonstrate that memory CD4+ T cells can be rendered anergic by presentation of low densities of agonist peptide–major histocompatibility complex complexes in vivo. We rule out other commonly accepted mechanisms for induction of T cell tolerance in vivo, such as deletion, ignorance, or immunosuppression. Anergy is the most likely mechanism because addition of interleukin 2–reversed anergy in specific T cells. Moreover, cytotoxic T lymphocyte antigen (CTLA)-4 plays a critical role in the induction of anergy because we observed that there was increased surface expression of CTLA-4 on anergized T cells, and that injection of anti–CTLA-4 blocking antibody restored anergy in vivo.


2010 ◽  
Vol 285 (40) ◽  
pp. 30427-30435 ◽  
Author(s):  
Katsuhiko Omoe ◽  
Wataru Nunomura ◽  
Hidehito Kato ◽  
Zhong-Juan Li ◽  
Osamu Igarashi ◽  
...  

1999 ◽  
Vol 190 (12) ◽  
pp. 1903-1908 ◽  
Author(s):  
You-Wen He ◽  
Michael J. Bevan

In a screen designed to identify genes that regulate T cell receptor (TCR)/CD3-mediated apoptosis, we found that high level expression of CD43 protected T cell hybridomas from activation-induced cell death. The protection appears to result from its capacity to block Fas-mediated death signals rather than from inhibition of the upregulation of Fas and/or Fas ligand after T cell stimulation. We found that peripheral CD4+ T cells can be divided into two subsets based on the level of CD43 surface expression. The CD4+CD43low subset exhibits a naive T cell phenotype, being CD62LhighCD45RBhighCD44low, whereas CD4+CD43high cells exhibit a memory phenotype, being CD62LlowCD45RBlowCD44high. Recent studies have demonstrated that engagement of TCR and Fas induces naive CD4+ T cells to undergo apoptosis, and the same treatment enhances the proliferation of memory CD4+ T cells. We confirm here that peripheral CD4+CD43high T cells are resistant to TCR/CD3-mediated cell death. These results suggest that the expression levels of CD43 on naive and memory CD4+ T cells determine their susceptibility to Fas-dependent cell death and that high level expression of CD43 may be used as a marker to define CD4+ memory T cells. Expression of CD43 provides a novel mechanism by which tumor cells expressing abnormally high levels of CD43 may escape Fas-mediated killing.


2019 ◽  
Vol 100 ◽  
pp. 1-6 ◽  
Author(s):  
Eduardo Beltrán ◽  
Xuan-Hung Nguyen ◽  
Clémence Quériault ◽  
Lucie Barateau ◽  
Yves Dauvilliers ◽  
...  

2000 ◽  
Vol 32 (2) ◽  
pp. 295-298 ◽  
Author(s):  
Y Iida ◽  
H Hirose ◽  
T Hirota ◽  
K Kanetake ◽  
Y Umeda ◽  
...  

1997 ◽  
Vol 27 (8) ◽  
pp. 2094-2101 ◽  
Author(s):  
Donna L. Farber ◽  
Oreste Acuto ◽  
Kim Bottomly

2021 ◽  
Vol 22 (5) ◽  
pp. 2713
Author(s):  
Sun-Hye Shin ◽  
Kyung-Ah Cho ◽  
Hee-Soo Yoon ◽  
So-Yeon Kim ◽  
Hee-Yeon Kim ◽  
...  

(1) Background: six mammalian ceramide synthases (CerS1–6) determine the acyl chain length of sphingolipids (SLs). Although ceramide levels are increased in murine allergic asthma models and in asthmatic patients, the precise role of SLs with specific chain lengths is still unclear. The role of CerS2, which mainly synthesizes C22–C24 ceramides, was investigated in immune responses elicited by airway inflammation using CerS2 null mice. (2) Methods: asthma was induced in wild type (WT) and CerS2 null mice with ovalbumin (OVA), and inflammatory cytokines and CD4 (cluster of differentiation 4)+ T helper (Th) cell profiles were analyzed. We also compared the functional capacity of CD4+ T cells isolated from WT and CerS2 null mice. (3) Results: CerS2 null mice exhibited milder symptoms and lower Th2 responses than WT mice after OVA exposure. CerS2 null CD4+ T cells showed impaired Th2 and increased Th17 responses with concomitant higher T cell receptor (TCR) signal strength after TCR stimulation. Notably, increased Th17 responses of CerS2 null CD4+ T cells appeared only in TCR-mediated, but not in TCR-independent, treatment. (4) Conclusions: altered Th2/Th17 immune response with higher TCR signal strength was observed in CerS2 null CD4+ T cells upon TCR stimulation. CerS2 and very-long chain SLs may be therapeutic targets for Th2-related diseases such as asthma.


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