By Dániel Lovas
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However, the presence of antibodies to double-stranded DNA may suggest a serious  Inﬂammation and Immunity form of SLE; these antibodies, if positively charged, may damage tissue directly. Throughout, I will refer to these antibodies as anti-DNA. Approximately half of SLE patients possess anti-DNA. By tracking their speciﬁc levels I can assess my patient’s response to therapy. , kidney) disease. Anti-Sm stands for a Mrs. Smith, in whom it was ﬁrst described. Antibodies to the Sm antigen are very speciﬁc for lupus (present in 20 to 30 percent of those with SLE) and are rarely observed in any other disease.
Natural killer lymphocytes promote inﬂammation and are not able to suppress or contain it. As a result, the body’s system of tolerance is disrupted so much that B cells are signaled to make antibodies to the patient’s own tissues, which are called autoantibodies. In other words, the normal immune surveillance system is altered in lupus, resulting in accelerated inﬂammatory responses and autoantibody formation; the autoantibodies, in turn, attack the body’s own cells and tissues. It is as if the body’s police force found itself unable to tolerate healthy, law-abiding cells and schemed to undermine them.
One of the best described is canine lupus, which is very similar to human lupus in its presentation and management. In the 1950s and 1960s occasional research studies utilized guinea pigs and rabbits, but these approaches have been abandoned. One laboratory has extensive experience inducing lupus in cats with an antithyroid preparation, but this has not been adopted as a research tool by other investigators. More than 95 percent of animal lupus research studies involve mice with lupus. WHY SHOULD WE STUDY ANIMAL MODELS OF LUPUS?