Hypothesis: Chlamydia trachomatis infection of the female genital tract is controlled by Type 2 immunity.
Vicetti Miguel RD1, Cherpes TL.
1Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Abstract
Chlamydia
trachomatis is an obligate intracellular bacterium sexually transmitted
to more than 90 million individuals each year. As this level of
infectivity implies, C. trachomatis is a successful human parasite; a
success facilitated by its ability to cause asymptomatic infection. Host
defense against C. trachomatis in the female genital tract is not well
defined, but current dogma suggests infection is controlled largely by
T(H)1 immunity. Conversely, it is well established that T(H)2 immunity
controls allergens, helminths, and other extracellular pathogens that
cause repetitive or persistent T cell stimulation but do not induce the
exuberant inflammation that drives T(H)1 and T(H)17 immunity. As C.
trachomatis persists in female genital tract epithelial cells but does
not elicit over tissue inflammation, we now posit that defense is
maintained by Type 2 immune responses that control bacterial growth but
minimize immunopathological damage to vital reproductive tract anatomy.
Evaluation of this hypothesis may uncover novel mechanisms by which Type
2 immunity can control growth of C. trachomatis and other intracellular
pathogens, while confirmation that T(H)2 immunity was selected by
evolution to control C. trachomatis infection in the female genital
tract will transform current research, now focused on developing
vaccines that elicit strong, and therefore potentially tissue
destructive, Chlamydia-specific T(H)1 immunity.
Copyright © 2012 Elsevier Ltd. All rights reserved.Med Hypotheses. 2012 Dec;79(6):713-6. doi: 10.1016/j.mehy.2012.07.032. Epub 2012 Sep 15.
http://www.sciencedirect.com/science/article/pii/S0306987712003568
Md. Rodolfo Vicetti. Ex-miembro del GII.
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