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Role of T Lymphocytes in the Pathogenesis ofChlamydiaDisease
Author(s) -
Joseph U. Igietseme,
Qing He,
Kahaliah Joseph,
Francis O. Eko,
Deborah Lyn,
Godwin A. Ananaba,
Angela Campbell,
Claudiu Bandea,
Carolyn M. Black
Publication year - 2009
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/605411
Subject(s) - immunity , chlamydia , immunology , vaccination , immune system , infertility , disease , pathogenesis , cellular immunity , chlamydia trachomatis , biology , medicine , pregnancy , genetics
Vaccines are needed to prevent the oculogenital diseases of Chlamydia trachomatis. Infected hosts develop immunity, although temporary, and experimental vaccines have yielded significant protective immunity in animal models, fueling the impetus for a vaccine. Because infections cause sequelae, the functional relationship between infection- and vaccine-induced immunity is unclear. We hypothesized that infection- and vaccine-induced immunity are functionally distinct, particularly in the ability to prevent sequelae. Chlamydia-immune mice, with immunity generated by either a previous infection or vaccination, exhibited a significant degree of protective immunity, marked by a lower-intensity, abbreviated course of infection. However, vaccinated mice were protected from infertility, whereas preinfected mice were not. Thus, infection-induced immunity does not prevent the pathologic process leading to infertility. Furthermore, T cell subsets, especially CD8 T cells, play a major role in Chlamydia-induced infertility. The results have important implications for the immunopathogenesis of chlamydial disease and new vaccine strategies.

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