MyD88: A Central Mediator of Corneal Epithelial Innate Immune Responses

摘要

Toll-like receptors (TLRs) are innate immune receptors that recognize both bacterial and viral pathogens. As the cornea may become infected by these pathogens, leading to vision loss, initial studies addressed the functional presence of TLRs within this tissue, thereby yielding a model of how immunological responses are initiated within the cornea. It has been determined that TLR2 and TLR9 are functionally necessary for the generation of inflammatory responses, as genetically deficient mice were impaired in their ability to respond to Pam 3 Cys and urtmethylated CpG DNA, respectively. MyD88 is a common adaptor molecule that is utilized by all TLRs, except TLR3. Consistent with this notion, it was shown that MyD88 is critical for the generation of TLR2-, TLR4-, and TLR9-induced keratitis, as defined by the production of CXC chemokines, neutrophil migration, and clinical disease (stromal haze and thickness).