ABSTRACT
The mechanisms of autoimmune disease are quite diverse. In some diseases, antibodies are of major importance in driving the pathogenesis of the disease; these include myasthenia gravis disease, Graves’ disease, Goodpasture’s syndrome, and autoimmune hemolytic anemia.1,2 In others T cells appear to be more important; these include multiple sclerosis and type I diabetes.3,4
However, in human diseases the mechanisms are usually complex, and there are usually huge gaps in our knowledge. For diseases where antibodies are important, there is often clear-cut evidence; for example, improvement upon removing the antibody by plasmapheresis (e.g. in Goodpasture’s syndrome), or mother-to-fetus transfer of disease due to transfer of pathogenic antibody. In other instances, if antibody-mediated pathology is not clearly defined, it is assumed that T cells are important. However, in human diseases, in contrast to animal models, the data needed to establish this point are usually circumstantial. In animal models transfer of T cells or antibody is possible to verify mechanisms. Collagen-induced arthritis, a model of rheumatoid arthritis (RA), is transferable by both T cells and antibodies.5 However, other models differ. K/BxN arthritis is transferable by serum or purified antibodies to glucose-6-phosphate isomerase.6
