Figure 1.

Model of C. trachomatis immunity and pathology. Following cervical infection, an early acute inflammatory response occurs, characterized by secretion of pro-inflammatory cytokines and recruitment of immune cells. Cytokine production by immune cells synergizes with ongoing immune responses that ultimately controls infection but also may cause pathology. C. trachomatis can ascend via the endometrium to the upper genital tract. As a consequence, local pro-inflammatory mediators and cytokines are produced. In an attempt to control the infection, Chlamydia-specific T cells and corresponding cytokines infiltrate the oviduct. These inflammatory responses, if persistent, may lead to fibrosis, scarring, and reproductive sequelae. Abbreviations: MMP, matrix metalloproteinases; SIgA, secretary immunoglobulin A; EBS, Chlamydia elementary bodies; MIP2, macrophage inflammatory protein-2.