Infections by Chlamydia are followed by a strong inflammatory response, which is necessary to eliminate the infection, but at the same time is responsible for the pathology of infection. Resistance of infected cells against apoptosis induced by external ligands, together with the effects of IFNγ secreted during infection, would be expected to contribute to persistence of infection. Secretion of TNFα plays an important role during clearance of the chlamydiae, but also triggers apoptosis of uninfected cells in infected tissues. Apoptosis of infected host-cells towards the end of the infection cycle is thought to participate in the release of chlamydiae from infected cells and propagation of the infection. Dysregulation of the apoptotic program during infection leads to a less efficient infection, but paradoxically, results in a higher inflammatory response and more severe pathology.