Chlamydia is an intracellular bacterium that infects many vertebrates, including humans. Previous studies have shown that interferon-γ(IFN-γ) plays an important role in defense against Chlamydia infection. IFN-γ-mediated anti-Chlamydia effector mechanisms may include the exhaustion of tryptophan, the induction of iron loss, and/or the activation of inducible nitric oxide synthase (iNOS). However, Chlamydia has evolved to develop mechanisms to escape IFN-γ functions. In this review, we will discuss IFN-γ-mediated effector mechanisms in the control of Chlamydia infection.
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