MHC Class-II-Restricted Antigen Presentation by Myelin Basic Protein-Specific CD4+ T Cells Causes Prolonged Desensitization and Outgrowth of CD4− Responders

2001 ◽  
Vol 212 (1) ◽  
pp. 51-62 ◽  
Author(s):  
Mark D. Mannie ◽  
Marcus S. Norris
2006 ◽  
Vol 38 (3) ◽  
pp. 755-756 ◽  
Author(s):  
C. Otto ◽  
A. Heeg ◽  
S. Kottenmeier ◽  
G.C. Tiurbe ◽  
A. Thiede ◽  
...  

Blood ◽  
2003 ◽  
Vol 101 (7) ◽  
pp. 2704-2710 ◽  
Author(s):  
Julia Y. S. Tsang ◽  
Jian Guo Chai ◽  
Robert Lechler

Antigen presentation by activated human and rat CD4+ T cells has long been known to induce hyporesponsiveness due to a combination of anergy and apoptosis. It has been assumed that no such phenomenon occurs in mice due to the inability of mouse T cells to synthesize major histocompatibility complex (MHC) class II molecules. There have been several recent descriptions of the transfer of molecules, including MHC molecules, from antigen-presenting cells (APCs) to T cells. Here, we describe the acquisition of MHC class II molecules by T-cell receptor (TCR)–transgenic T cells and T-hybridoma cells following culture with APCs. Acquisition was markedly enhanced by T-cell activation either due to cognate recognition of antigen or anti-CD3 activation. When activation was induced by antigen recognition, preferential acquisition of complexes of class II molecules displaying cognate peptide was observed; in contrast, following activation by anti-CD3 the acquisition of class II molecules was MHC unrestricted. T cells that had acquired MHC class II:peptide complexes were able to act as APCs and induced proliferation and interleukin-2 secretion by resting T cells. However, when activated T cells that had acquired MHC class II:peptide complexes engaged in T:T interactions, this led to an increase in apoptosis and the induction of hyporesponsiveness. These results raise the possibility that the acquisition of MHC class II:peptide complexes by T cells during an immune response may serve to limit clonal expansion, including that induced by alloantigen following tissue or stem cell transplantation.


2021 ◽  
pp. ji2000498
Author(s):  
Melanie Lancien ◽  
Geraldine Bienvenu ◽  
Sonia Salle ◽  
Lucile Gueno ◽  
Magalie Feyeux ◽  
...  

2020 ◽  
Vol 204 (6) ◽  
pp. 1621-1629 ◽  
Author(s):  
Kyung-Jin Cho ◽  
Satoshi Ishido ◽  
Laurence C. Eisenlohr ◽  
Paul A. Roche

1998 ◽  
Vol 187 (7) ◽  
pp. 1037-1046 ◽  
Author(s):  
Mark T. Heise ◽  
Megan Connick ◽  
Herbert W. Virgin

CD4 T cells and interferon γ (IFN-γ) are required for clearance of murine cytomegalovirus (MCMV) infection from the salivary gland in a process taking weeks to months. To explain the inefficiency of salivary gland clearance we hypothesized that MCMV interferes with IFN-γ induced antigen presentation to CD4 T cells. MCMV infection inhibited IFN-γ–induced presentation of major histocompatibility complex (MHC) class II associated peptide antigen by differentiated bone marrow macrophages (BMMφs) to a T cell hybridoma via impairment of MHC class II cell surface expression. This effect was independent of IFN-α/β induction by MCMV infection, and required direct infection of the BMMφs with live virus. Inhibition of MHC class II cell surface expression was associated with a six- to eightfold reduction in IFN-γ induced IAb mRNA levels, and comparable decreases in IFN-γ induced expression of invariant chain (Ii), H-2Ma, and H-2Mb mRNAs. Steady state levels of several constitutive host mRNAs, including β-actin, cyclophilin, and CD45 were not significantly decreased by MCMV infection, ruling out a general effect of MCMV infection on mRNA levels. MCMV effects were specific to certain MHC genes since IFN-γ–induced transporter associated with antigen presentation (TAP)2 mRNA levels were minimally altered in infected cells. Analysis of early upstream events in the IFN-γ signaling pathway revealed that MCMV did not affect activation and nuclear translocation of STAT1α, and had minor effects on the early induction of IRF-1 mRNA and protein. We conclude that MCMV infection interferes with IFN-γ–mediated induction of specific MHC genes and the Ii at a stage subsequent to STAT1α activation and nuclear translocation. This impairs antigen presentation to CD4 T cells, and may contribute to the capacity of MCMV to spread and persist within the infected host.


2014 ◽  
Vol 133 (2) ◽  
pp. AB292
Author(s):  
Lyndsey Muehling ◽  
Rachana Agrawal ◽  
Julia Wisniewski ◽  
Paul Wright ◽  
William W. Kwok ◽  
...  

2002 ◽  
Vol 169 (4) ◽  
pp. 2172-2179 ◽  
Author(s):  
Ryusuke Omiya ◽  
Chantal Buteau ◽  
Hiroya Kobayashi ◽  
Carlos V. Paya ◽  
Esteban Celis
Keyword(s):  
T Cells ◽  

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