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Query: UMLS:C0026918 (Mycobacterium)
 52,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:In-vitro lymphoproliferative response to Mycobacterium leprae of HLA-D-identical siblings of lepromatous leprosy patients. 7 15

Leprosy is a spectral disease in which immune responses to Mycobacterium leprae correlate with the clinical, bacteriological and histopathological manifestations of disease, so study of its pathology provides insights into immunoregulatory mechanisms in man. At the tuberculoid pole, patients have few lesions in the skin which contain rare organisms and are able to mount strong cell-mediated immune responses to M. leprae antigens. In contrast, at the lepromatous pole, patients have disseminated skin lesions containing large numbers of acid-fast bacilli and are selectively unresponsive to antigens of M. leprae. M. leprae-induced suppressor cells derived from peripheral blood have been reported to be active in vitro, yet their in vivo significance has remained unclear. Because the focal point of the immune response to M. leprae is the skin lesion consisting of lymphocytes and macrophages, we have recently developed methods for isolating lymphocytes from skin biopsies of leprosy patients. We report here that two T8 clones derived from lepromatous leprosy skin biopsies, in the presence of lepromin, suppress concanavalin A (Con-A) responses both of peripheral blood mononuclear cells and of T4 clones in an HLA-D (HLA, histocompatibility locus antigen)-restricted manner. Moreover, these T8 clones suppressed responses of HLA-D-matched, but not HLA-D-mismatched antigen-responsive T4 clones to M. leprae antigens, indicating that T-cell suppression is major histocompatibility complex (MHC)-restricted at some level in man.
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PMID:Genetically restricted suppressor T-cell clones derived from lepromatous leprosy lesions. 294 80

Sixteen healthy siblings were identified as HLA-D-identical to 12 borderline lepromatous or polar lepromatous leprosy patients by the absence of a mixed lymphocyte reaction (MLR). The peripheral blood mononuclear cells (PBM) of the healthy siblings showed a lymphoproliferative response (delta cpm) to Mycobacterium leprae antigens which was about fivefold or more greater than that of the lepromatous patients. Lepromatous PBM, with or without mitomycin C treatment, were co-cultured with a constant number of normal PBM. In other experiments the two cell types were co-cultured in various proportions, with the total cell number kept constant. Neither approach revealed suppressor cells in lepromatous PBM capable of suppressing the lymphoproliferative response to M. leprae. On the contrary, we found that lepromatous PBM can respond to M. leprae antigens if the sensitized lymphocyte is provided by mitomycin-C treated normal PBM. Additionally, experiments in which isolated adherent cells and non-adherent cells of sibling pairs were recombined failed to reveal a defect in the M. leprae antigen-presenting function of lepromatous adherent cells. Since we found no evidence that sensitized cells are present in lepromatous PBM with their function unexpressed (due to a monocyte defect) or suppressed (due to suppressor cells), we conclude that lepromatous patients simply lack sufficient numbers of antigen-specific T lymphocytes to initiate a lymphoproliferative response to M. leprae antigens. The reason for their absence remains an important unanswered question.
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PMID:Studies on the defect in cell-mediated immunity in lepromatous leprosy using HLA-D-identical siblings. Absence of circulating suppressor cells and evidence that the defect is in the T-lymphocyte, rather than the monocyte, population. 617 16

Evidence for the presence of Mycobacterium leprae reactive T cells in many lepromatous leprosy (LL) patients was obtained using in vitro antigen-induced lymphoproliferative responses. (1) Co-cultures of T enriched cells from LL patients when combined with 2 h adherent cells (AC) from HLA-D compatible tuberculoid leprosy individuals showed significant levels of 3H-thymidine incorporation in the presence of soluble and integral M. leprae antigens. (2) More interestingly, autologous T cell + AC co-cultures also showed significant improvement in antigen-induced lymphoproliferation in nine of 16 lepromatous patients. Insignificant improvement was observed in similar co-cultures of tuberculoid leprosy patients. (3) Addition of exogenous, purified human interleukin-2 (IL-2) to antigen stimulated PBMC from some lepromatous patients showed the best improvement in terms of overall 3H-thymidine incorporation, indicating that lepromatous patients possess T cells which can differentiate to an IL-2 responsive state. Significantly, the level of proliferation varied within the group. A proportion of clinically similar lepromatous patients failed to show improvement by any of the above methods.
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PMID:Evidence for the presence of M. leprae reactive T lymphocytes in patients with lepromatous leprosy. 639 62

Peripheral blood monocytes from polar lepromatous leprosy (LL) patients were unable to support Mycobacterium leprae-induced in vitro lymphoproliferation of HLA-D-matched T cells from tuberculoid leprosy subjects, whereas those from responder individuals were able to do so. Monocyte-rich adherent cells from untreated LL patients released de novo soluble factors which inhibited antigen-induced lymphoproliferation to a greater extent and mitogenic responses to a lesser extent. Suppressive activity varied in different LL patients. However, the degree of suppression was similar in soluble factors obtained de novo and after treatment of adherent cells with heat-killed and freshly extracted, cryopreserved M. leprae. Treated patients showed less inhibition with de novo released soluble factors (27 +/- 7.7%) as compared to parallel soluble factors obtained after antigen treatment (44 +/- 4.8%) or with de novo soluble factors from untreated LL patients (62 +/- 14.2%). Similar supernatants from tuberculoid individuals showed no or insignificant effects on antigen-induced lymphoproliferation. The suppressive activity of LL soluble factors was produced for up to 72 h, was heat stable at 56 degrees C for 30 min, was indomethacin resistant, and resided in the greater than 25,000 molecular weight fraction.
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PMID:Monocyte-derived soluble suppressor factor(s) in patients with lepromatous leprosy. 660 32

Of 30 bacterial species tested 18 stimulated DNA synthesis in human blood lymphocytes. The maximum response was after 3-4 days of culture suggesting a mitogenic effect. This was confirmed by the induction of polyclonal antibody production shown by a plaque assay. Most bacterial species increased the DNA synthesis in B-enriched lymphocytes and unseparated lymphocytes but had negligible activity on T-enriched lymphocytes. Among bacteria with a mitogenic effect and ability to induce polyclonal antibody production are Staphylococcus aureus, Haemophilus influenzae, Mycobacterium tuberculosis, Neisseria gonorrhoeae, Streptococcus group A and Streptococcus pneumoniae. In an attempt to define structure (s) on the B-lymphocyte surface responsible for the lymphocyte stimulation the binding of IgD, IgM, and HLA-A, -B and HLA-D antigens to different bacterial species was investigated. A high IgD binding to N. catarrhalis and H. influenzae and a moderate binding of IgD to streptococci was found. Binding studies employing radiolabelled IgD Fab- and Fc-fragments indicated that the binding probably involves the CHl-region of the IgD molecule. Three purified radiolabelled myeloma IgM M-components were all shown to be efficiently bound to many bacteria indicating that a part of the IgM molecule other than the antigen-combining site can be involved in attachment to bacteria. Highly purified detergent-solubilized HLA-A, -B and HLA-D antigens, when separately incorporated into liposomes, were bound efficiently to two strains of N. catarrhalis and to one strain of H. influenzae weakly to one strain of E. coli, but not at all to another strain E. coli. Preliminary experiments indicate that these bacteria-immunoglobulin and bacteria-HLA-antigen interactions lead to lymphocyte stimulation.
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PMID:Bacteria-immunoglobulin-lymphocyte interactions--new aspects. 693 74