RESISTANCE TO HGCL2-INDUCED AUTOIMMUNITY IN HAPLOTYPE-HETEROZYGOUS MICE IS AN INTRINSIC PROPERTY OF B-CELLS

Citation
Ga. Hanley et al., RESISTANCE TO HGCL2-INDUCED AUTOIMMUNITY IN HAPLOTYPE-HETEROZYGOUS MICE IS AN INTRINSIC PROPERTY OF B-CELLS, The Journal of immunology (1950), 161(4), 1998, pp. 1778-1785
Citations number
43
Categorie Soggetti
Immunology
ISSN journal
00221767
Volume
161
Issue
4
Year of publication
1998
Pages
1778 - 1785
Database
ISI
SICI code
0022-1767(1998)161:4<1778:RTHAIH>2.0.ZU;2-Y
Abstract
Exposure to low doses of mercury chloride induces autoantibodies to th e nucleolar protein fibrillarin in H-2(s), but not in H-2(b), mice. Su rprisingly, F-1 crosses between resistant and sensitive haplotypes are resistant. Previously, we have shown that the resistance in these F-1 mice was due to coexpression of the resistant class II allele, Using adoptive transfer techniques we have examined several mechanisms by wh ich the resistant haplotype could be down-regulating the antifibrillar in response in F-1 (s/b) mice. Similar to other autoimmune models, mer cury-induced autoimmunity requires cognate MHC-restricted T cell help. The absence of autoantibody production in F-1 mice was not due to a d ifference in thymic education or to the absence of antifibrillarin-spe cific T cell help. These results suggest that the resistance is due to an intrinsic property of the haplotype-heterozygous B cells.