[Circulating immune complexes in lepromatous leprosy patients].
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The type of leprosy which develops after infection with Mycobacterium leprae is influenced by the presence or absence of HLA-DR3, as has been demonstrated in an ethnic group originating from Surinam. In the present study we investigated in this same ethnic group the role of HLA-DR, and of HLA-DR3 in particular, in monocyte-T cell interactions during leprosy specific proliferative responses in vitro. HLA-DR3 heterozygous T cells from tuberculoid leprosy patients were cultured with antigen and either HLA-DR3 positive or HLA-DR3 negative homozygous HLA-DR compatible allogeneic monocytes as antigen presenting cells (APCs). T cell proliferative responses with DR3 homozygous monocytes as APCs, were observed to be decreased as compared to T cell proliferative responses with DR3 negative homozygous monocytes as APCs. Furthermore, although the leprosy specific monocyte-T cell interactions were shown to be restricted for HLA-DR, in the anti-MLW-1 response HLA-DR3 appeared to function as a restricting element poorly or not at all. These observations may imply, that an in vitro correlate has been found for an (HLA associated) genetic control of leprosy in vivo.
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Some references of the history of Mitsuda reaction and its antigen, as well as for the results and significance of this unique reaction are presented. In spite of the great advances of modern immunology. Mitsuda reaction is still the best method for the diagnosis of the forms of hanseniasis and for the prognosis of the disease in patients and in healthy persons.
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Two aspects of the phagocytic process in normal and lepromatous polymorphonuclears (PMN) and monocytes (MN) were studied. These aspects were endocytosis and adherence to surfaces. These 2 phenomena are closely related to each other and to the whole phagocytic process as they depend on membrane activity. It was found that both lepromatous phagocytes (PMN and MN) show, on the average, a depressed ability to endocytose opsonized Mycobacterium lepraemurium when compared to normal phagocytes. This impairment, however, does not seem to be related to intrinsic defects in the phagocytic cells themselves but to the presence in lepromatous serum of factors that interfere with the endocytic function. This conclusion was drawn from the fact that lepromatous serum causes a similar diminution in the endocytic ability of normal phagocytes. On the other hand, lepromatous plasma but not indeterminate leprosy nor normal plasmas interfere with the capacity of PMN leukocytes to adhere in vitro to plastic surfaces. These impairments in the phagocytic function might help to better understand the depressed overall inflammatory responses observed in vivo in lepromatous patients with a long-lasting disease.