Journal
NATURE IMMUNOLOGY
Volume 5, Issue 5, Pages 516-523Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1063
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Funding
- NIAID NIH HHS [AI 07386, AI 48125, AI37562, AI 13600, R01 AI037562] Funding Source: Medline
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The mouse protein Qa-1 (HLA-E in humans) is essential for immunological protection and immune regulation. Although Qa-1 has been linked to CD8 T cell-dependent suppression, the physiological relevance of this observation is unclear. We generated mice deficient in Qa-1 to develop an understanding of this process. Qa-1-deficient mice develop exaggerated secondary CD4 responses to foreign and self peptides. Enhanced responses to proteolipid protein self peptide were associated with resistance of Qa-1-deficient CD4 T cells to Qa-1-restricted CD8 T suppressor activity and increased susceptibility to experimental autoimmune encephalomyelitis. These findings delineate a Qa-1-dependent T cell-T cell inhibitory interaction that prevents the pathogenic expansion of autoreactive CD4 T cell populations and consequent autoimmune disease.
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