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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1989-6-9
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pubmed:abstractText |
Analysis of tissue lesions of the major reactional states of leprosy was undertaken to study the immune mechanisms underlying regulation of cell-mediated immunity and delayed-type hypersensitivity (DTH) in man. In situ hybridization hybridization of reversal reaction biopsy specimens for INF-gamma mRNA expression revealed a 10-fold increase in specific mRNA-containing cells over that observed in unresponsive lepromatous patients. Expression of huHF serine esterase, a marker for T cytotoxic cells, were fourfold increased in reversal reaction and tuberculoid lesions above that detected in unresponsive lepromatous individuals. Immunohistology of reversal reactions confirmed a selective increase of Th and T cytotoxic cells in the cellular immune response. Of interest, the microanatomic location of these serine esterase mRNA-containing cells was identical to the distribution of CD4+ cells. Analysis of erythema nodosum leprosum (ENL) lesions revealed differences in the underlying immune processes in comparison with reversal reaction lesions. Although phenotypic Th cells predominated in ENL lesions, IFN-gamma and serine esterase gene expression were markedly reduced. We suggest that reversal reactions represent a hyperimmune DTH response characterized by a selective increase of CD4+ IFN-gamma producing cells and T cytotoxic cells, which result in the clearing of bacilli and concomitant tissue damage. In contrast, ENL reactions may be viewed as a transient diminution of Ts cells and activity leading to a partial and transient augmentation in cell-mediated immunity, perhaps sufficient to result in antibody and immune complex formation, but insufficient to clear bacilli from lesions.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2523952-1009681,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2523952-2416837,
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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 |
May
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pubmed:issn |
0022-1007
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
169
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pubmed:owner |
NLM
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pubmed:authorsComplete |
N
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pubmed:pagination |
1565-81
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2523952-Esterases,
pubmed-meshheading:2523952-Gene Expression Regulation,
pubmed-meshheading:2523952-Humans,
pubmed-meshheading:2523952-Hypersensitivity, Delayed,
pubmed-meshheading:2523952-Immunohistochemistry,
pubmed-meshheading:2523952-Interferon-gamma,
pubmed-meshheading:2523952-Leprosy,
pubmed-meshheading:2523952-Nucleic Acid Hybridization,
pubmed-meshheading:2523952-RNA, Messenger,
pubmed-meshheading:2523952-T-Lymphocytes,
pubmed-meshheading:2523952-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:2523952-T-Lymphocytes, Regulatory
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pubmed:year |
1989
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pubmed:articleTitle |
Analysis of naturally occurring delayed-type hypersensitivity reactions in leprosy by in situ hybridization.
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pubmed:affiliation |
Department of Pathology, 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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