Chlamydia trachomatis-Infected Epithelial Cells and Fibroblasts Retain the Ability To Express Surface-Presented Major Histocompatibility Complex Class I Molecules

Abstract

ABSTRACTThe obligate intracellular bacterial pathogenChlamydia trachomatisis the causative agent of a variety of infectious diseases such as trachoma and sexually transmitted diseases. In infected target cells,C. trachomatisreplicates within parasitophorous vacuoles and expresses the protease-like activity factor CPAF. Previous studies have suggested that CPAF degrades the host transcription factors RFX5 and NF-κB p65, which are involved in the regulation of constitutive and inducible expression of major histocompatibility complex class I (MHC I). It was speculated thatChlamydiasuppresses the surface presentation of MHC I in order to evade an effective immune response. Nevertheless, a recent study suggested that RFX5 and NF-κB p65 may not serve as target substrates for CPAF-mediated degradation, raising concerns about the proposed MHC I subversion byChlamydia. Hence, we investigated the direct influence ofChlamydiaon MHC I expression and surface presentation in infected host cells. By using nine different human cells and cell lines infected withC. trachomatis(serovar D or LGV2), we demonstrate that chlamydial infection does not interfere with expression, maturation, transport, and surface presentation of MHC I, suggesting functional antigen processing in bacterium-infected cells. Our findings provide novel insights into the interaction of chlamydiae with their host cells and should be taken into consideration for the design of future therapies and vaccines.