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Resistance to HgCl₂-Induced Autoimmunity in Haplotype-Heterozygous Mice Is an Intrinsic Property of B Cells¹

Gregory A. Hanley^*, Joel Schiffenbauer and Eric S. Sobel^2,

^* Department of Physiological Sciences, College of Veterinary Medicine, and Department of Medicine, Division of Rheumatology and Clinical Immunology, College of Medicine, University of Florida, Gainesville, FL 32610

Exposure to low doses of mercury chloride induces autoantibodies to the nucleolar protein fibrillarin in H-2^s, but not in H-2^b, mice. Surprisingly, F₁ crosses between resistant and sensitive haplotypes are resistant. Previously, we have shown that the resistance in these F₁ mice was due to coexpression of the resistant class II allele. Using adoptive transfer techniques we have examined several mechanisms by which the resistant haplotype could be down-regulating the antifibrillarin response in F₁ (s/b) mice. Similar to other autoimmune models, mercury-induced autoimmunity requires cognate MHC-restricted T cell help. The absence of autoantibody production in F₁ mice was not due to a difference in thymic education or to the absence of antifibrillarin-specific T cell help. These results suggest that the resistance is due to an intrinsic property of the haplotype-heterozygous B cells.

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