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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibodies, Antinuclear / biosynthesis
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Autoimmune Diseases / genetics*
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Autoimmune Diseases / immunology
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Autoimmune Diseases / pathology
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B-Lymphocyte Subsets / immunology*
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B-Lymphocyte Subsets / metabolism
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Cell Nucleolus / immunology
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Chromosomal Proteins, Non-Histone / immunology
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Crosses, Genetic
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Haplotypes
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Heterozygote*
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Histocompatibility Antigens Class II / genetics
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Histocompatibility Antigens Class II / immunology
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Humans
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Immunity, Innate / drug effects
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Immunity, Innate / genetics
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Lymphocyte Cooperation / genetics
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Mercuric Chloride / immunology*
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Mercuric Chloride / pharmacology
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Mice
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Mice, Inbred C57BL
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Radiation Chimera / genetics
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Radiation Chimera / immunology
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T-Lymphocytes, Helper-Inducer / immunology
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T-Lymphocytes, Helper-Inducer / metabolism
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Thymus Gland / immunology
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Thymus Gland / pathology
Substances
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Antibodies, Antinuclear
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Chromosomal Proteins, Non-Histone
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Histocompatibility Antigens Class II
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fibrillarin
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Mercuric Chloride