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Biomedical subjects

A Belehu

Publications and source records attributed to A Belehu.

43 records · Page 3Linked to original sources
PubMed1978

In-vitro lymphoproliferative response to Mycobacterium leprae of HLA-D-identical siblings of lepromatous leprosy patients.

Lymphoproliferative responses to Mycobacterium leprae and P.P.D. were measured in 23 lepromatous and borderline lepromatous leprosy patients and in 27 of their normal siblings. At the same time siblings HLA-D-identical with the patients were identified by the absence of a mixed-lymphocyte reaction. The 7 siblings who were HLA-identical to lepromatous patients responded as well to M. leprae as did the 20 HLA-non-identical normal siblings. In contrast, 22 of the 23 lepromatous patients failed to respond to M. leprae but responded normally to P.P.D. The specific unresponsiveness of lepromatous patients thus does not result from an HLA-linked genetic defect and the defective cell-mediated immune response to M. leprae seems to be acquired, not inherited. Lepromatous patients may be high responders to antigens shared by M. leprae and other microorganisms in whom a strong antibody response has blocked the induction of an M. leprae-specific-cell-mediated immune response.

Adolescent↗
PubMed1976

Establishment of cutaneous Leishmania enriettii infection in hamsters.

A model of a self-healing type of cutaneous leishmaniasis was established in hamsters using the guinea pig parasite Leishmania enriettii. L. enriettii was passaged several times in hamsters without losing its infectivity for guinea pigs or for hamsters. The course of the infection in hamsters resembled that of guinea pigs, with the exception that the lesion at the site of parasite inoculation did not ulcerate and no metastatic lesions developed spontaneously. Moreover, unlike guinea pigs, infected or recovered hamsters were skin test unresponsive to various preparations of L. enriettii antigens. However, histological examination of draining lymph nodes showed features of a cell-mediated immune response, and in vitro inhibition of macrophage migration was demonstrable using peritoneal exudate cells from recovered animals and specific leishmanial antigen. Antibody was demonstrable by indirect immunofluorescence starting 1 week after infection. Recovered animals were immune to reinfection; however, the passive transfer of peritoneal exudate cells or serum from recovered animals did not confer protection against L. enriettii infection in normal animals.

Animals↗
PubMed1976

Influence of rodent malaria on the course of Leishmania enriettii infection of hamsters.

Plasmodium yoelii infection was established in hamsters, and the effect of this type of malaria on concurrent Leishmania enriettii infection was examined. It was found that the course of the L. enriettii infection was affected by P. yoelii and that this effect depended on the relative timing of the two infections. A chronic malarial infection with Plasmodium berghei was also established in hamsters, and this was found to affect the course of a concurrent L. enriettii infection in a similar manner to P. yoelii. These results are discussed in relation to current knowledge of the immunosuppressive effects of plasmodia.

Animals↗
PubMed1976

Modification of cutaneous leishmaniasis in the guinea-pig by cyclophosphamide.

Pretreatment of guinea-pigs with cyclophosphamide (Cy) (300 mg/kg) 3 days before cutaneous infection with Leishmania enriettii caused an increased intensity of the lesion at the site of infection and an increase in the incidence of widespread metastases. Decreased levels of circulating antibody were found from the first to fourth week after infection. Decreased delayed type hypersensitivity could only be detected beyond 4 weeks. Peritoneal macrophages obtained form guinea-pigs 3 days after Cy pretreatment showed increase rather than decreased ability to phagocytose L. enriettii. Phagocytosis of L. enriettii by peritoneal macrophages obtained from guinea-pigs pretreated with Cy 24 days previously was normal. It is suggested that more attention should be taken of antibody levels during the early phase of infection and that control of infection could be due to a synergism between antibody and cell-mediated immunity. Upset in the balance by suppression of either function might lead to the development of widespread metastatic lesions.

Animals↗
PubMedDate not supplied

Antigen-specific suppressor cells in subclinical leprosy infection.

A two-stage in-vitro culture system was used to assay cells which suppress the lympho-proliferative response to Mycobacterium leprae (ML). Responses to ML, purified protein derivative of tuberculin, and streptokinase-streptodornase were preferentially suppressed by mitomycin-treated cells which had been primed with the same antigen in a 7-day primary culture. Healthy subjects exposed to leprosy for more than 3 years showed strong suppression of the response to ML antigens (11 of 12 showed more than 40% suppression), whereas those exposed for 3 months to 3 years showed much less suppression (12 of 15 showed less than 40% suppression). The in-vitro generation of strong ML-specific suppression may reflect the maturation of a well-regulated and protective immune response. However, premature induction and in-vivo activation of these suppressor cells could predispose to disseminated (lepromatous) forms of leprosy. With this assay it would be possible to assess the ability of proposed leprosy vaccines to engage strongly the regulatory network controlling the immune response to ML in the same way as long-term exposure to the natural infection.

Adolescent↗