| Autor: |
Hu D; Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA., Ikizawa K, Lu L, Sanchirico ME, Shinohara ML, Cantor H |
| Jazyk: |
angličtina |
| Zdroj: |
Nature immunology [Nat Immunol] 2004 May; Vol. 5 (5), pp. 516-23. Date of Electronic Publication: 2004 Apr 18. |
| DOI: |
10.1038/ni1063 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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