title: Learning from lesions: patterns of tissue inflammation in leprosy.
abstract: The clinical forms of leprosy constitute a spectrum that correlates closely with the degree of cell-mediated immunity. Patients with tuberculoid leprosy develop strong cell-mediated responses and have only a few, localized lesions, whereas patients with multibacillary lepromatous leprosy are specifically unresponsive to antigens of Myobacterium leprae. T cells of the CD4+ subset predominate in tuberculoid lesions, whereas CD8+ cells predominate in lepromatous lesions. Monoclonal antibodies that distinguish subpopulations of CD4+ and CD8+ cells were used to analyze the distribution of T cells infiltrating lesions across the disease spectrum. In lepromatous lesions, T cells of T-suppressor phenotype (9.3-) were the predominant CD8+ cells and suppressor/inducer cells (2H4+, Leu-8+) represented half of the CD4+ subset. In tuberculoid lesions, helper T cells (CD4+4B4+) outnumbered suppressor/inducer T cells by 14:1, compared with a ratio of 1.2:1 in peripheral blood. Analysis of the precursor frequency of antigen-reactive T cells permitted us to estimate that there was a 100-fold enrichment of T cells able to proliferate in response to M. leprae antigens in tuberculoid lesions (2/100), when compared with blood from the same patients. The methods used here to characterize the T-lymphocyte subsets and frequency of antigen-reactive T cells in leprosy may be useful in analyzing immunological reactions occurring in lesions of other inflammatory and autoimmune diseases.
authors.affiliation: Section of Dermatology, University of Southern California School of Medicine, Los Angeles 90033.
authors.forename: R L
authors.initials: RL
authors.lastname: Modlin
authors.forename: J
authors.initials: J
authors.lastname: Melancon-Kaplan
authors.forename: S M
authors.initials: SM
authors.lastname: Young
authors.forename: C
authors.initials: C
authors.lastname: Pirmez
authors.forename: H
authors.initials: H
authors.lastname: Kino
authors.forename: J
authors.initials: J
authors.lastname: Convit
authors.forename: T H
authors.initials: TH
authors.lastname: Rea
authors.forename: B R
authors.initials: BR
authors.lastname: Bloom
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D002478:Cells, Cultured; D006099:Granuloma / Q000473:pathology; D006801:Humans; D007111:Immunity, Cellular; D007249:Inflammation; D007376:Interleukin-2 / Q000494:pharmacology; D007918:Leprosy / Q000276:immunology / Q000473:pathology*; D008213:Lymphocyte Activation; D010641:Phenotype; D013601:T-Lymphocytes / Q000145:classification* / Q000187:drug effects / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D000945:Antigens, Differentiation, T-Lymphocyte; D007376:Interleukin-2