Mozes E, Kohn L D, Hakim F, Singer D S
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD 20892.
Science. 1993 Jul 2;261(5117):91-3. doi: 10.1126/science.8316860.
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.
实验性系统性红斑狼疮（SLE）可通过用携带共同独特型（16/6Id）的抗DNA人单克隆抗体免疫小鼠来诱导。这些小鼠产生针对16/6Id的抗体、针对DNA的抗体以及针对核抗原的抗体。随后，出现SLE的表现，包括白细胞减少、蛋白尿和肾脏中的免疫复合物沉积。相比之下，用16/6Id免疫后，缺乏主要组织相容性复合体（MHC）I类分子的小鼠产生了针对16/6Id的抗体，但未产生针对DNA或核抗原的抗体。此外，它们没有出现上述任何临床表现。这些结果揭示了MHC I类分子在自身免疫性SLE诱导中的意外功能。
