02966nas a2200457   4500000000100000008004100001260001300042653002600055653002400081653001600105653001100121653003800132653001100170653001600181653002100197653001100218653002300229653001200252653002300264653002500287653003100312653002600343653003200369653001500401653002400416653001700440653002800457100001400485700001100499700001300510700001500523700001500538700001400553700001400567245026000581856004100841300001100882490000700893520159400900022001402494       1992                            d  c1992 Jun10aAntibodies, Bacterial10aAntigens, Bacterial10aBCG Vaccine10aBrazil10aEnzyme-Linked Immunosorbent Assay10aFrance10aGlycolipids10aHealth Personnel10aHumans10aImmunity, Cellular10aleprosy10aMilitary Personnel10aMycobacterium leprae10aMycobacterium tuberculosis10aOccupational Diseases10aSensitivity and Specificity10aSkin Tests10aSpecies Specificity10aTuberculosis10aTuberculosis, Cutaneous1 aDavid H L1 aPapa F1 aCruaud P1 aBerlie H C1 aMaroja M F1 aSalem J I1 aCosta M F00aRelationships between titers of antibodies immunoreacting against glycolipid antigens from Mycobacterium leprae and M. tuberculosis, the Mitsuda and Mantoux reactions, and bacteriological loads: implications in the pathogenesis, epidemiology and serodiagn  uhttp://ila.ilsl.br/pdfs/v60n2a07.pdf  a208-240 v603 a<p>Analysis of cell-mediated immunity [(CMI) as judged from the Mantoux, Fernandez, and Mitsuda reactions and the presence of granulomas in biopsy material] against humoral immunity (measurements of anti-PGL-I, PGL-Tb1, and SL-IV IgG and IgM antibody titers by ELISA) were performed in selected human populations. The investigations yielded data indicating that humoral (B-cell) responses preceded protective CMI in both tuberculosis and leprosy. The B-cell responses were unrelated to (unfavorable) cell-mediated delayed-type hypersensitivity (DTH). Notwithstanding the difficulty in inferring sequential events from studies in humans, it was shown that in humoral responses there was an initial rise of specific IgM immunoglobulins that switched afterward to IgG production during subclinical tuberculosis and leprosy infections. In patent tuberculosis disease the IgM-to-IgG switch was observed in the majority of patients; in patent leprosy disease the switch was impaired in the majority of patients. The clinical, immunological, and laboratory data indicated that the B-cell responses were suppressed as protective CMI was re-established in the patients during the protracted subclinical infection. According to the data, the diagnosis of subclinical tuberculosis and leprosy may be accomplished using ELISA. The yearly risk of tuberculosis in apparently healthy persons but with significant antibody titers was estimated at 44%; the yearly risk for leprosy has not yet been established. The clinical, epidemiologic, and diagnostic implications of these findings are discussed.</p>
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