Premium
Studies in Knockout Mice Reveal that Anti‐Chlamydial Protection Requires TH1 Cells Producing IFN‐γ: Is this True for Humans?
Author(s) -
JOHANSSON M.,
SCHÖN K.,
WARD M.,
LYCKE N.
Publication year - 1997
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1997.d01-167.x
Subject(s) - chlamydiae , chlamydia trachomatis , biology , immunology , obligate , chlamydia , immune system , immunity , innate immune system , knockout mouse , intracellular parasite , infertility , microbiology and biotechnology , gene , virology , genetics , pregnancy , ecology
Chlamydia trachomatis is one of the major causes of infertility and preventable blindness in the world. The organism is of particular interest from an immunological point of view because it is one of the few obligate intracellular bacterial pathogens. There is some evidence that repeated infections in humans stimulate protective immunity. However, until recently, it was unclear which components of the adaptive immune system give rise to protection. Studies in gene knockout mice reported here and elsewhere now give a coherent and cogent picture of the importance of the Th1 response, in particular IFN‐γ, for the localization and eradication of C. trachomatis genital tract infection. The key questions still to be addressed are the identity of the IFN‐γ responsive cells and whether the mouse is truly representative of host protection against chlamydiae in humans.