期刊
JOURNAL OF IMMUNOLOGY
卷 171, 期 9, 页码 4613-4620出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.171.9.4613
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R56AI044924, R01AI044924, R01AI042284, R21AI042284] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK058765] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI42284, AI44924] Funding Source: Medline
- NIDDK NIH HHS [DK58765] Funding Source: Medline
Th cell differentiation is a critical event in the adaptive immune response. C57BL strains develop predominant Th1 responses while BALB/c develops a predominant Th2 response. To identify quantitative trait loci controlling this variation, we performed Th1/Th2 differentiation assays of F, X BALB/c progeny. A single strong quantitative trait locus was identified on chromosome 18, with weaker effects detectable on chromosomes 5, 12, and 14. By preparing a congenic BALB.B10.D2c18 strain, we were able to demonstrate that this single locus was sufficient to repolarize spleen cell cultures. This difference was not due to intrinsic differences in CD4(+) T cells. Rather, introgression of the chromosome 18 locus into BALB/c disrupted Va14Ja18 NKT cell homeostasis resulting in the almost complete absence of this T cell subset. Taken together, these data indicate that genes within chromosome 18 control strain-dependent development of Va14Ja18 NKT cells.
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