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The Y chromosome from autoimmune BXSB/MpJ mice induces a lupus‐like syndrome in (NZW × C57BL/6)F 1 male mice, but not in C57BL/6 male mice
Author(s) -
Izui Shozo,
Higaki Megumu,
Morrow Dwight,
Merino Ramon
Publication year - 1988
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830180612
Subject(s) - c57bl/6 , biology , systemic lupus erythematosus , immunology , y chromosome , ratón , microbiology and biotechnology , genetics , medicine , gene , disease
Abstract The Y chromosome of the BXSB mouse has been shown to be responsible for the acceleration of lupus‐like autoimmune syndrome in inbred BXSB mice and in their F 1 hybrids with NZB or NZW mice. To further define the role of this as yet unidentified gene linked to the BXSB Y chromosome, designated Yaa (Y chromosome‐linked autoimmune acceleration), the Y chromosome was transferred from the BXSB strain to nonautoimmune C57BL/6 (B6) mice. The effect of the Yaa gene on the autoanti‐body formation and the development of glomerulonephritis was investigated in B6 mice and in their F 1 hybrids with NZW mice. The presence of the BXSB Y chromosome was not able to induce significant autoimmune responses in B6 mice. However, (NZW × B6)F 1 males bearing the BXSB Y chromosome developed a severe lupus‐like autoimmune syndrome, as documented by the production of anti‐DNA antibodies and gp70‐anti‐gp70 immune complexes and the development of lethal lupus nephritis. Both sexes of (NZW × B6)F 1 hybrids without the BXSB Y chromosome were essentially normal. Our results suggest that (a) the BXSB Y chromosome by itself is not sufficient to initiate autoimmune responses in nonautoimmune B6 mice, and (b) it is able to induce autoimmune responses in mice potentially capable of developing the disease, but whose autosomal abnormality by itself is not sufficient to develop autoimmune diseases.