Literature DB >> 3133391

T-cell subpopulations, expression of interleukin-2 receptor, and production of interleukin-2 and gamma interferon in human American cutaneous leishmaniasis.

M Castes1, M Cabrera, D Trujillo, J Convit.   

Abstract

Leukocyte subpopulations, the expression of the interleukin-2 (IL-2) receptor, and the production of IL-2 and gamma interferon (IFN-gamma) were studied in the peripheral blood mononuclear cells of American cutaneous leishmaniasis patients that had been stimulated in vitro with either leishmanial antigen or mitogen (phytohemagglutinin M). The 75 patients examined were classified as having either the localized (LCL; 66 patients), mucocutaneous (MCL; 5 patients), or the rare diffuse (DCL; 4 patients) form of the disease. Patients with DCL, who are characterized by their defective cell-mediated immune response to leishmanial antigen, failed to express the IL-2 receptor and did not produce IFN-gamma when exposed to the antigen but did so when stimulated by phytohemagglutinin M. Both LCL and MCL patients showed strong proliferative responses to leishmanial antigen; these were by far the greatest in MCL patients. Both groups had significantly increased IL-2 receptor expression and IFN-gamma production after exposure to either antigen or mitogen, and these were highest in the MCL patients. Concerning the leukocyte subpopulations evaluated (CD2, CD4, CD8, CD20, MO2), the most significant findings were a decrease of both CD4+ cells and the CD4/CD8 ratio in MCL patients compared with the other groups. Considering IL-2 production, in response to phytohemagglutinin M both MCL and LCL patients showed amounts of IL-2 comparable to those of the controls. Our results help explain the anergy of T cells from DCL patients to leishmanial antigen, which could lead to a defective production of IFN-gamma and possibly contribute to their incapacity to kill the Leishmania parasite. Concerning MCL patients, the significantly increased expression of IL-2 receptor, decreased expression of the CD4 (helper-inducer of suppression) phenotype, and elevated IFV-gamma production might partially explains the state of hypersensitivity and mucosal damage exhibited by these patients.

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Year:  1988        PMID: 3133391      PMCID: PMC266563          DOI: 10.1128/jcm.26.6.1207-1213.1988

Source DB:  PubMed          Journal:  J Clin Microbiol        ISSN: 0095-1137            Impact factor:   5.948


  31 in total

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4.  Interleukin 2 receptor blockade by anti-Tac antibody inhibits IFN-gamma induction.

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5.  Monoclonal antibodies to human immune interferon and their application for affinity chromatography.

Authors:  J Le; B S Barrowclough; J Vilcek
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6.  Cell mediated immunity in American cutaneous and mucosal leishmaniasis.

Authors:  E M Carvalho; W D Johnson; E Barreto; P D Marsden; J L Costa; S Reed; H Rocha
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7.  Reversible defect in antigen-induced lymphokine and gamma-interferon generation in cutaneous leishmaniasis.

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8.  Use of monoclonal antibodies as sensitive and specific probes for biologically active human gamma-interferon.

Authors:  T W Chang; S McKinney; V Liu; P C Kung; J Vilcek; J Le
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9.  In situ characterization of the cellular immune response in American cutaneous leishmaniasis.

Authors:  R L Modlin; F J Tapia; B R Bloom; M E Gallinoto; M Castes; A J Rondon; T H Rea; J Convit
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10.  Regulation of IFN-gamma induction in human peripheral blood cells by exogenous and endogenously produced interleukin 2.

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6.  CD8+ T cells as a source of IFN-γ production in human cutaneous leishmaniasis.

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7.  Determination of the cytokine profile in American cutaneous leishmaniasis using the polymerase chain reaction.

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