For many years immune response in leprosy has been studied. Since 1960 several reports dealing with humoral immunity have been described in the literature. Different autoantibody rates occur in leprosy. There is an increase in the prevalence of autoantibodies in elderly patients with long standing disease, in lepromatous leprosy and in those with reactional states. The differences in rates among various studies are attributed to different methods and variations among patient samples concerning age, gender, polar forms, therapy and other elements. The prevalence of numerous antibodies, immune complexes, cryoglobulins and complement levels have been studied by many authors. This also highlights the importance of the more recent reviews of anti-Mycobacterium leprae glycolipid antibodies such as the anti-phenolic glycolipid-I antibodies in which titers are variable and depend on genetic factors.

Anticardiolipin antibodies (ACA) were assayed by ELISA in 73 patients with rheumatoid arthritis. Twelve (16.48%) patients showed levels of ACA three standard deviations above the value of the control group and were considered positive; these patients were compared to the group with ACA within the normal levels regarding the following clinical and laboratorial characteristics: spontaneous abortions, central nervous system involvement, systematization and activity of disease, alterations in platelet counts, presence of antinuclear antibodies and rheumatoid factor. Significant statistical association could be demonstrated between systematization and presence of antinuclear antibodies (ANA) and positiveness to ACA (IgG, IgM or both). These findings might indicate that ACA in patients with RA could have relevance to morbidity of disease or perhaps to its pathogenesis.

Possible mechanisms of chronic leprosy-related arthritisMicrobial agents induce arthritis through mechanisms such as direct infiltration of tissue and by inducing autoimmune phenomena. The mechanisms involved in this last type of arthritis have been investigated. In experimental models of adjuvant and reactive arthritis, the involvement of T cells and in some cases mycobacteria in the development of arthritis have been confirmed. Cross-reactivity boetween the 65 kD mycobacterial protein and cartilage proteoglycans has been postulated as a possible mechanism. In this study, chronic peripheral arthritis was observed in patients with Hansen's disease, in patients with resolved Hansen's and in those with paucibacillary forms. This arthritis was not related to reactional states (erythema nodosum leprosum and reversal reaction), in contrast to several reports in the literature. The mechanisms by which microbes could induce chronic arthritis are discussed herein.