Leprosy Masquerading as Systemic Rheumatic Diseases.

Rheumatologic manifestations not only are encountered in leprosy but also can be the first and even the sole presenting manifestation. The hallmark of leprosy is skin and peripheral nerve affection; however, it can affect a wide range of other organs, with the joints being the commonest. We have searched PubMed with the key words leprosy, arthritis, vasculitis, rheumatic diseases, and autoantibodies in a proper combination. Relevant studies were retrieved from scanning of their abstracts. The relevant references provided in these articles were also selected and reviewed. We summarize the clinical and laboratory manifestations that make leprosy masquerade as a systemic rheumatic disease. Moreover, we report 4 Egyptian patients who presented with rheumatologic manifestations, namely, arthritis and vasculitis that turned out to be leprosy related.

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Immunotherapy of tuberculosis with Mycobacterium leprae Hsp65 as a DNA vaccine triggers cross-reactive antibodies against mammalian Hsp60 but not pathological autoimmunity.

Despite substantial efforts in recent years toward the development of new vaccines and drugs against tuberculosis (TB), success has remained elusive. Immunotherapy of TB with mycobacterial Hsp65 as a DNA vaccine (DNA-hsp65) results in a reduction of systemic bacterial loads and lung tissue damage, but the high homology of Hsp65 with the mammalian protein raises concern that pathological autoimmune responses may also be triggered. We searched for autoimmune responses elicited by DNA-hsp65 immunotherapy in mice chronically infected with TB by evaluating the humoral immune response and comprehensive histopathology using stereology. Cross-reactive antibodies between mycobacterial and mammalian Hsp60/65 were detected; however, no signs of pathological autoimmunity were found up to 60 days after the end of the therapy.

A symbiotic concept of autoimmunity and tumour immunity: lessons from vitiligo.

Vitiligo is a skin disease in which melanocytes (MCs) are eradicated from lesional epidermis, resulting in disfiguring loss of pigment. MCs are destroyed by MC-reactive T cells, as well as other non-immune and immune components. Similarities exist between the autoimmunity observed in vitiligo and the tumour immunity observed in melanoma immuno-surveillance. An analysis of these mechanisms might lead to the development of new therapies for both vitiligo and melanoma.

Raised agalactosyl IgG and antimycobacterial humoral immunity in Takayasu's arteritis.

OBJECTIVE: Takayasu's arteritis is an inflammatory occlusive disease of the aorta and its main branches of unknown etiology. Some suggested causes include inapparent infection with Mycobacterium tuberculosis, or autoimmunity evoked by this organism. We have therefore sought links with mycobacterial disease. METHODS: We assayed the % agalactosyl IgG, antibody to a tuberculosis-specific 38 kDa protein, and antibody to the mycobacterial 65 kDa heat shock protein (HSP), in patients with active or inactive Takayasu's arteritis, in whom the diagnosis of tuberculosis was excluded. The results were compared with findings in tuberculosis (positive controls), normal donors and patients with Wegener's granulomatosis. RESULTS: The % agalactosyl IgG in patients with active arteritis was in the range previously seen only in rheumatoid arthritis, Crohn's disease, and the mycobacterioses. Similarly, significantly raised antibody to the purified 38-kDa protein of M. tuberculosis, and to the 65-kDa HSP of M. leprae, was found in 78% of patients with Takayasu's arteritis, and the levels were higher in those with active disease. CONCLUSION: These results suggest that Takayasu's arteritis particularly clearly illustrates the occasional relationship between mycobacteria and diseases of superficially autoimmune pathogenesis.

An hypothesis to explain why cell-mediated immunity alone can contain infections by certain intracellular parasites and how immune class regulation of the response against such parasites can be subverted.

Cells with a low density of parasite-specific antigens on their surface are postulated to be susceptible to a cell-mediated attack but not to effector mechanisms normally activated following the binding of specific antibody to the infected cell. It is further postulated that such infected cells normally induce a cell-mediated response, and that cells infected with slow-growing intracellular parasites have a low density of parasite-specific antigens on their surface. Despite these general postulates, cell-mediated immunity is not invariably induced following natural infection by certain slow-growing parasites, such as those responsible for leprosy, tuberculosis, and the leishmaniases, and antibody can be induced that is exclusive of a strong, cell-mediated response. It is proposed that certain events in such cases subvert the normal regulatory processes that control the class of immunity induced. In these cases, the parasite-infected cells, bearing a low representation of parasite antigens, induce antibody even though they are not susceptible to antibody-dependent effector mechanisms, and so they are not eliminated. In this case, chronic infection and uncontrolled growth of the parasite occurs, often with fatal consequences.

Autoimmunity associated with infection: leprosy, acute rheumatic fever and Lyme disease.

This review examines the links between autoimmunity and three common infectious diseases. These disorders are associated with a variety of clinical and serological autoimmune phenomena. In addition they might conceivably trigger autoimmune diseases themselves. Mechanisms that may be responsible for these links, including molecular mimicry, are explored.