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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1988-3-21
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pubmed:abstractText |
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.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-2426181,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-2426597,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-2887618,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-2942780,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-2944966,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-2952513,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-2952854,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-3155770,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-3157750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-3936719,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-5950347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-6216407,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-6219136,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-6327818,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-6763002,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-7009746,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3257577-80324
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1213-7
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:3257577-Antibodies, Monoclonal,
pubmed-meshheading:3257577-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:3257577-Cells, Cultured,
pubmed-meshheading:3257577-Granuloma,
pubmed-meshheading:3257577-Humans,
pubmed-meshheading:3257577-Immunity, Cellular,
pubmed-meshheading:3257577-Inflammation,
pubmed-meshheading:3257577-Interleukin-2,
pubmed-meshheading:3257577-Leprosy,
pubmed-meshheading:3257577-Lymphocyte Activation,
pubmed-meshheading:3257577-Phenotype,
pubmed-meshheading:3257577-T-Lymphocytes
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pubmed:year |
1988
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pubmed:articleTitle |
Learning from lesions: patterns of tissue inflammation in leprosy.
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pubmed:affiliation |
Section of Dermatology, University of Southern California School of Medicine, Los Angeles 90033.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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