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Induction of abnormal Chlamydia trachomatis by exposure to interferon-gamma or amino acid deprivation and comparative antigenic analysis

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UNSPECIFIED (2001) Induction of abnormal Chlamydia trachomatis by exposure to interferon-gamma or amino acid deprivation and comparative antigenic analysis. MICROBIAL PATHOGENESIS, 30 (5). pp. 299-309. doi:10.1006/mpat.2000.0433

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Official URL: http://dx.doi.org/10.1006/mpat.2000.0433

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Abstract

Abnormal forms of Chlamydia trachomatis have been induced in vitro by a variety of methods including nutrient deprivation, addition of cytokines and addition of antibiotics. These forms have been shown to have altered morphology and infectivity and have been implicated in persistent infections in vivo although there is little direct evidence for their presence. Likely sites for abnormal forms in vivo are the genital tract and the synovial tissue of reactive arthritis patients, and T cells isolated from the synovial tissue have been shown to be specific for chlamydial antigens, in particular the Hsp60. Since T cell specificity is so important in reactive arthritis disease the antigenic composition of abnormal forms induced by Interferon-gamma and amino acid deprivation has been examined by western blotting in two strains of C. trachomatis belonging to different biovars. The degree of abnormality of the organisms was found to increase as the treatments became more severe. No simple patterns of antigenic changes were found and differences in the antigenic composition were seen in abnormal forms induced by the different treatments and also in the different strains. (C) 2001 Academic Press.

Item Type: Journal Article
Subjects: Q Science > QR Microbiology > QR180 Immunology
Q Science > QR Microbiology
Journal or Publication Title: MICROBIAL PATHOGENESIS
Publisher: ACADEMIC PRESS LTD
ISSN: 0882-4010
Official Date: May 2001
Dates:
DateEvent
May 2001UNSPECIFIED
Volume: 30
Number: 5
Number of Pages: 11
Page Range: pp. 299-309
DOI: 10.1006/mpat.2000.0433
Publication Status: Published

Data sourced from Thomson Reuters' Web of Knowledge

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