Role of toll-like receptors in immune responses to chlamydial infections

Chlamydiae are important human pathogens which are leading causative agents for a variety of disease conditions including ocular, respiratory and sexually transmitted diseases, thus causing significant morbidity worldwide. Many of the human diseases caused by Chlamydia species are considered to be immunopathologically mediated. Toll like receptors (TLRs) have emerged as one of the major components of the immune system. Recognition of pathogen associated molecular patterns (PAMPs) by TLRs results in the activation of signaling events that induce the expression of effector molecules such as cytokines and chemokines which control the activation of adaptive immune responses. The precise immune mechanisms involved in resistance or pathogenesis to chlamydial infection, especially in the TLR signaling and downstream events during the innate phase of infection initiating the adaptive immune responses remains largely unknown. This review focuses on elaborating the current knowledge on the role of TLRs in immune responses to chlamydial infection. Although chlamydial components like lipopolysaccharide (LPS) and chlamydial heat shock protein 60 (cHSP60) are recognized by TLR4, the intact organisms stimulates the innate immune cells through TLR2, which also plays an important role as a PRR for Chlamydia. While the individual role of different TLRs such as TLR2, TLR4 and TLR9 in chlamydial infection is becoming delineated, studies have demonstrated the essential role of the TLR adapter molecule MyD88 in the generation of immune responses to Chlamydia infection. Given that there is no effective vaccine available for Chlamydia till date, a better understanding of the immunological and molecular mechanisms mediated by TLRs will greatly aid in possibly exploiting these molecules as immunotherapeutic targets.