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Review
. 2004 Nov;114(9):1218-21.
doi: 10.1172/JCI23152.

Qa-1 Restriction of CD8+ Suppressor T Cells

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Free PMC article
Review

Qa-1 Restriction of CD8+ Suppressor T Cells

Stefanie Sarantopoulos et al. J Clin Invest. .
Free PMC article

Abstract

There is increasing evidence that the immune response can be inhibited by several T cell subsets, including NK T cells, CD25+CD4+ T cells, and a subpopulation of CD8+ T cells. Animal model studies of multiple sclerosis have suggested an important role for suppressor CD8+ T cells in protection against disease recurrence and exacerbation. The molecular lynchpin of CD8+ suppressive activity is the murine MHC molecule Qa-1, termed HLA-E in humans. Here we summarize findings from work on Qa-1 that have begun to delineate suppressor CD8+ T cells and their mechanisms of action in the context of self tolerance and autoimmune disease.

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Figure 1
Figure 1
Engagement of Qa-1 by the TCR and by CD94/NKG2A. (A) Presentation of Qa-1–bacterial GroEL peptide by a DC following Salmonella infection to CD8+ T cells, where the receptor is a TCR, leads to CTL responses. (B) Presentation of Qa-1–self peptides by activated CD4+ T cells to CD8+ T cells, where the receptor is a TCR, leads to the development of Qa-1–restricted suppressor CD8+ T cells. (C) Engagement of CD94/NKG2A receptors on CD8+ T cells with a DC can inhibit either TCR-mediated CTL responses specific for Qa-1–foreign peptide ligands and/or TCR-mediated suppressive responses specific for Qa-1–self peptide ligands. This NKG2A-dependent interaction may regulate expression of suppressor or cytotoxic CD8+ T cells through inhibition of cellular activation or diminished AICD.

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