Immunological aspects of leprosy with special reference to autoimmune diseases

Leprosy, particularly lepromatous leprosy, is associated with a multitude of (auto) immune aberrations, and its clinical features also have much in common with the collagen diseases. Immunopathological studies of the 2 groups of diseases may thus elucidate the basic mechanisms of both.The reported evidence for a genetically determined hyporeactivity of cell-mediated (CM) immunity in lepromatous subjects is reviewed; most, but not all, of the findings fit such a hypothesis well. The possibility remains that the observed hyporeactivities may be secondary to direct effects of Mycobacterium leprae. Evidence for a general hyperreactivity of the antibody-mediated (AM) immunity in lepromatous leprosy is then reviewed and considered to be fragmentary.The concept and general criteria of autoimmunity are discussed briefly and the high incidence in lepromatous leprosy of various (auto)immune aberrations, resembling those in systemic lupus erythematosus (SLE) and in rheumatoid arthritis is reviewed. Although autoantibodies are not likely to be directly deleterious to the host, immune complexes containing autoantibodies may be pathogenic.Mixed cryoimmunoglobulins, consisting of 2 (IgG-IgM or IgG-IgA) or 3 immunoglobulins, and occasionally also containing measurable amounts of complement components, have recently been encountered in SLE and its variants and also in a number of microbial diseases with autoimmune features (syphilis, streptococcal nephritis and endocarditis, mononucleosis, Mycoplasma pneumoniae pneumonia). They may represent circulating immune complexes, analogous to the IgM (IgA) rheumatoid factors in combination with their IgG reactants. In leprosy also, the existence of pathogenic immune complexes is indirectly suggested by mixed cryoglobulinemia and further by a number of other features reviewed in this article.