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A Murine Locus on Chromosome 18 Controls NKT Cell Homeostasis and Th Cell Differentiation ¹

Feng Zhang^*,, Zhiyan Liang^,, Naoto Matsuki, Luc Van Kaer, Sebastian Joyce, Edward K. Wakeland^, and Thomas M. Aune^2,*,

^* Division of Rheumatology, Department of Medicine, and Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232; Simmon’s Arthritis Research Center, Department of Medicine, and Center for Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75235

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 F₁ 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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