Resistance of MHC class I-deficient mice to experimental systemic lupus erythematosus
- 2 July 1993
- journal article
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 261 (5117) , 91-93
- https://doi.org/10.1126/science.8316860
Abstract
Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal antibody to DNA that bears a common idiotype (16/6Id). These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE.Keywords
This publication has 6 references indexed in Scilit:
- Beta 2-microglobulin-, CD8+ T-cell-deficient mice survive inoculation with high doses of vaccinia virus and exhibit altered IgG responses.Proceedings of the National Academy of Sciences, 1992
- Susceptibility of β2-microglobulin-deficient mice to Trypanosoma cruzi infectionNature, 1992
- Normal Development of Mice Deficient in β 2 M, MCClass I Proteins, and CD8 + T CellsScience, 1990
- β2-Microglobulin deficient mice lack CD4−8+ cytolytic T cellsNature, 1990
- Induction of a systemic lupus erythematosus-like disease in mice by a common human anti-DNA idiotype.Proceedings of the National Academy of Sciences, 1988
- Idiotypic cross-reactions of monoclonal human lupus autoantibodies.The Journal of Experimental Medicine, 1983