Immune deficit in patients with lepromatous leprosy: its nature and relation to genetic factors, spectrum, and duration of the illness.
Cell-mediated immunity or hypersensitivity to M. leprae and other unrelated antigens, such as tuberculin and dinitrochlorobenzene, was studied in 73 leprosy patients of different histopathologic types. It was found that specific as well as nonspecific anergy intensified as the disease spectrum shifted from the tuberculoid toward the lepromatous immunologic pole. Within the lepromatous group, the impairment of cellular immunity became more pronounced as the bacillary load increased. It was found that the impairment of the cell-mediated immunity towards antigens other than M. leprae became more severe as the duration of the illness increased. Late lepromin responsiveness, which is the hallmark of resistance of an individual to M. leprae, may be absent even before the onset of clinical illness. Its deficit seems to be primary and has a genetic predisposition.
D000328:Adult; D002648:Child; D004137:Dinitrochlorobenzene / Q000494:pharmacology; D005260:Female; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000139:chemically induced / Q000276:immunology*; D007916:Lepromin / Q000276:immunology; D007918:Leprosy / Q000235:genetics / Q000276:immunology*; D008297:Male; D013997:Time Factors; D014373:Tuberculin / Q000276:immunology
D004137:Dinitrochlorobenzene; D014373:Tuberculin; D007916:Lepromin