Journal
JOURNAL OF IMMUNOLOGY
Volume 182, Issue 11, Pages 7163-7171Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0803933
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Funding
- National Institute of Allergy and Infectious Disease, National Institutes of Health [R01 AI050072]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI050072] Funding Source: NIH RePORTER
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Essential NK cell-mediated murine CMV (MCMV) resistance is under histocompatibility-2(k) (H-2(k)) control in MA/My mice. We generated a panel of infra-H2(k) recombinant strains from congenic C57L.M-H2(k/b) (MCMV resistant) mice for precise genetic mapping of the critical interval. Recombination breakpoint sites were precisely mapped and MCMV resistance/susceptibility traits were determined for each of the new lines to identify the MHC locus. Strains C57L.M-H2(k)(R7) (MCMV resistant) and C57L.M-H2(k)(R2) (MCMV susceptible) are especially informative; we found that allelic variation in a 0.3-megabase interval in the class 1 D locus confers substantial difference in MCMV control phenotypes. When NK cell subsets responding to MCMV were examined, we found that Ly49G2(+) NK cells rapidly expand and selectively acquire an enhanced capacity for cytolytic functions only in C57L.M-H2(k)(R7). We further show that depletion of Ly49G2(+) NK cells before infection abrogated MCMV resistance in C57L.M-H2(k)(R7). We conclude that the MHC class I D locus prompts expansion and activation of Ly49G2(+) NK cells that are needed in H-2(k) MCMV resistance. The Journal of Immunology, 2009, 182: 7163-7171.
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