151. Resistance to HgCl2-induced autoimmunity in haplotype-heterozygous mice is an intrinsic property of B cells.
- Author
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Hanley GA, Schiffenbauer J, and Sobel ES
- Subjects
- Animals, Antibodies, Antinuclear biosynthesis, Autoimmune Diseases immunology, Autoimmune Diseases pathology, B-Lymphocyte Subsets metabolism, Cell Nucleolus immunology, Chromosomal Proteins, Non-Histone immunology, Crosses, Genetic, Haplotypes, Histocompatibility Antigens Class II genetics, Histocompatibility Antigens Class II immunology, Humans, Immunity, Innate drug effects, Immunity, Innate genetics, Lymphocyte Cooperation genetics, Mercuric Chloride pharmacology, Mice, Mice, Inbred C57BL, Radiation Chimera genetics, Radiation Chimera immunology, T-Lymphocytes, Helper-Inducer immunology, T-Lymphocytes, Helper-Inducer metabolism, Thymus Gland immunology, Thymus Gland pathology, Autoimmune Diseases genetics, B-Lymphocyte Subsets immunology, Heterozygote, Mercuric Chloride immunology
- Abstract
Exposure to low doses of mercury chloride induces autoantibodies to the nucleolar protein fibrillarin in H-2s, but not in H-2b, 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.
- Published
- 1998