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

The obligate intracellular bacterial pathogen Chlamydia trachomatis is the causative agent for a variety of infectious diseases such as trachoma and sexually transmitted diseases. In infected target cells C. trachomatis replicates within parasitophorous vacuoles and expresses the protease-like activity factor CPAF. Previous studies suggested that CPAF degrades the host transcription factors RFX5 and NFκB p65, which are involved in the regulation of constitutive and inducible expression of major histocompatibility complex class I (MHC I). It was speculated that chlamydia suppresses the surface presentation of MHC I in order to evade an effective immune response. Nevertheless, a recent study suggested that RFX5 and NFκB p65 may not serve as target substrates for CPAF-mediated degradation raising concerns about the proposed MHC I subversion by chlamydia. Hence, we investigated the direct influence of chlamydia on MHC I expression and surface presentation in infected host cells. Using nine different human cells and cell lines infected with C. trachomatis (serovars 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 bacteria-infected cells. Our findings provide novel insights into the interaction of chlamydia with their host cells and should be taken into consideration for the design of future therapies and vaccines.



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