The role of IFN-γ in the outcome of chlamydial infection

Chlamydia are intracellular bacteria which infect many vertebrates, including humans. They cause a myriad of severe diseases, ranging from asymptomatic infection to pneumonia, blindness or infertility. IFN-γ plays an important role in defense against acute infection and in the establishment of persistence. Chlamydia have evolved mechanisms to escape IFN-γ functions. IFN-γ-mediated effector mechanisms may involve effects on the metabolism of tryptophan or iron, on the inducible NO synthase (iNOS), on the secretion of chemokines and adhesion molecules or on the regulation of T-cell activities. IFN-γ is secreted by the innate and the adaptive arms of the immune system. Within the former, Chlamydia-infected macrophages express IFN-γ that in turn mediates resistance to infection. IFN-α/β are pivotal for both IFN-γ- and iNOS-mediated resistance to chlamydial infection in macrophages. Different cells and regulatory mechanisms complement each other to provide sufficient levels of IFN-gamma, a key player in the defense against chlamydial infection. However, Chlamydia has found its way to subvert IFN-gamma-mediated surveillance.