The Role That the Functional Asp299Gly Polymorphism in the Toll‐Like Receptor–4 Gene Plays in Susceptibility toChlamydia trachomatis–Associated Tubal Infertility

These findings show that innate immune response—and, in part, adaptive immune response, through increased production of INF-g—limits the initial reproduction of the parasite and subsequently provokes its elimination

Servaas A. Morré

2003

Scholarcy highlights

  • Taken together, these findings show that innate immune response—and, in part, adaptive immune response, through increased production of INF-g—limits the initial reproduction of the parasite and subsequently provokes its elimination
  • Activation of NK cells and T cells by IL-18 and IL-12 is able to produce tumor necrosis factor–a, which cooperates with INF-g to lead to resolution of malarial infection
  • In severe P. falciparum malaria, including cerebral malaria, increased production of transforming growth factor-b may be associated with anti-inflammatory effects, through inhibition or decrease of proinflammatory cytokines such as IL-18 and IL-12 during the early phase of immune activation
  • High levels of TGF-b up-regulate the antiinflammatory cytokine response, which provokes reduced production of IL-12, IL18, and INF-g, with increased and persistent production of TNF-a, a series of events that is responsible for severe P. falciparum malaria infection as well as for cerebral malaria
  • We had previously shown that gd T cells are a significant source of interferon–g, and, more recently, we have demonstrated that human NK cells can be activated by Plasmodium falciparum–infected red blood cells to produce IFN-g
  • To further assess the role that the Asp299Gly polymorphism in the Toll-like receptor 4 gene plays in human gram-negative infections, we investigated its relation with C. trachomatis infection and tubal infertility
  • Despite both the reported functional significance of Asp299Gly and the reported associations described elsewhere, we remain unconvinced that it has any effect on the manifestation of gram-negative infections, and we consider that inefficient Toll-like receptor 4 signaling may not be rate limiting during human responses to natural LPS-driven diseases

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