Identification of a particular B cell alloantigen associated with susceptibility to lepromatous leprosy

Patarroyo, Manuel E.; Molina, Elizabeth; Londoño, F; Bernal, Dolores; Caro, Lucien; Velasques, A; Y, Silva; Moya, Raquel; Guevara, José Ramón Vielma; Meness, A; González, Marcos

doi:10.5935/0305-7518.19810064

Cited by 2 publications

(2 citation statements)

References 2 publications

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“…Macrophages from six contacts showed an ability to react to M. leprae similar to macrophages from lepromatous patients (unpublished data). The association between genetic markers and susceptibility to lepromatous leprosy has also been demonstrated by other workers (6,9).…”

Section: Infection Of Macrophages From Normal Subjectssupporting

confidence: 68%

Alterations in the membrane of macrophages from leprosy patients

Birdi¹,

Mistry²,

Mahadevan³

et al. 1983

Infect Immun

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Macrophage cultures pulsed with viable Mycobacterium leprae were assessed for erythrocyte rosetting in three groups of individuals, i.e., normal subjects, and tuberculoid and lepromatous patients. Of these, only the lepromatous group showed a reduction in rosetting ability after infection with M. leprae. The specificity of such a reduction pattern was confirmed by using various mycobacteria to infect the macrophages. A threshold effect was noted in all three groups. Although a reduction was obtained in the amount of rosetting of macrophages from lepromatous patients with 10(4) acid-fast bacilli per culture, tuberculoid and normal macrophages resisted such an effect with as large a dose as 20 X 10(6) to 30 X 10(6) and 30 X 10(6) bacilli per culture, respectively. The M. leprae-caused alterations in macrophages from lepromatous patients were reversible by treatment with trypsin and colchicine. Cytochalasin B and Tween 80 were unable to alter the pattern. Treatment of cells with neuraminidase was inconclusive since it enhanced rosetting values of both control and infected cultures. These manipulations were significant in elucidating the target point of the host (macrophage) and parasite (M. leprae) interaction and in delineation of the external and internal effects upon the macrophages. Both M. leprae and macrophages were participants in Fc reduction, as treatment of the former with rifampicin and of the latter with cyclocheximide significantly augmented the rosetting ability. In conclusion, it appears that M. leprae, upon entering a lepromatous macrophage, initiates the production of a protein which acts via the microtubules to alter membrane topography. It is possible that the altered membrane prevents effective macrophage-lymphocyte interaction. This could be one of the mechanisms by which cell-mediated immunity is suppressed in lepromatous leprosy.

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Section: Infection Of Macrophages From Normal Subjectssupporting

confidence: 68%

Alterations in the membrane of macrophages from leprosy patients

Birdi¹,

Mistry²,

Mahadevan³

et al. 1983

Infect Immun

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“…These data are being reanalyzed using the maximum-likelihood complex segregation analysis routine GENPED [Russell, personal communication]. Patarroyo et al [1981] studied several large, multiplex kindreds with leprosy living in Colombia and also concluded that the segregation pattern of a particular B-cell alloantigen that was strongly associated with lepromatous leprosy was consistent with autosomal dominant inheritance. The overall segregation ratio was estimated to be 0.43.…”

Section: Discussionmentioning

confidence: 99%

Segregation analysis of leprosy in families of northern Thailand

Wagener

Schauf

Nelson

et al. 1988

Genetic Epidemiology

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Sixty-three families with multiple instances of leprosy were identified through a major leprosy treatment center in northern Thailand. Complex segregation analyses for single major genes or polygenic inheritance were performed using the maximum-likelihood routine POINTER to determine the most likely etiologic model of genetic susceptibility. Liability differences between men and women were considered in these models. When individuals were considered to be affected because they had any form of leprosy, a generalized major gene model with nearly dominant parameters on the liability scale, but additive penetrances, was found to be the most likely. When only those individuals who had tuberculoid forms of leprosy were considered to be affected, a recessive model was found to be the most likely; however, the discrimination between various models was poor. Further analyses are necessary to delineate genetic mechanisms to explain these apparently divergent results. In particular, methods of testing two locus models should be considered.

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Identification of a particular B cell alloantigen associated with susceptibility to lepromatous leprosy

Cited by 2 publications

References 2 publications

Alterations in the membrane of macrophages from leprosy patients

Alterations in the membrane of macrophages from leprosy patients

Segregation analysis of leprosy in families of northern Thailand

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