Hanley G A, Schiffenbauer J, Sobel E S
Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville 32610, USA.
J Immunol. 1998 Aug 15;161(4):1778-85.
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.
低剂量氯化汞暴露可诱导H-2s小鼠而非H-2b小鼠产生针对核仁蛋白纤维原蛋白的自身抗体。令人惊讶的是，抗性和敏感单倍型之间的F1杂交后代具有抗性。此前，我们已经表明这些F1小鼠的抗性是由于抗性II类等位基因的共表达。我们利用过继转移技术研究了抗性单倍型下调F1（s/b）小鼠抗纤维原蛋白反应的几种机制。与其他自身免疫模型类似，汞诱导的自身免疫需要同源MHC限制的T细胞辅助。F1小鼠中自身抗体产生的缺失并非由于胸腺教育的差异或抗纤维原蛋白特异性T细胞辅助的缺失。这些结果表明，抗性是由于单倍型杂合B细胞的内在特性。
