title: Chlamydia trachomatis-infected epithelial cells and fibroblasts retain the ability to express surface-presented major histocompatibility complex class I molecules.
abstract: The obligate intracellular bacterial pathogen Chlamydia trachomatis is the causative agent of 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 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 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 NF-κB 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. By using nine different human cells and cell lines infected with C. 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.
authors.affiliation: Institute of Immunology, Federal Research Institute of Animal Health, Friedrich Loeffler Institute, Greifswald, Isle of Riems, Germany.
authors.forename: Danny
authors.initials: D
authors.lastname: Kägebein
authors.forename: Melanie
authors.initials: M
authors.lastname: Gutjahr
authors.forename: Christina
authors.initials: C
authors.lastname: Große
authors.forename: Annette B
authors.initials: AB
authors.lastname: Vogel
authors.forename: Jürgen
authors.initials: J
authors.lastname: Rödel
authors.forename: Michael R
authors.initials: MR
authors.lastname: Knittler
mesh_terms: D045744:Cell Line, Tumor; D002690:Chlamydia Infections / Q000276:immunology*; D002692:Chlamydia trachomatis / Q000276:immunology*; D004847:Epithelial Cells / Q000276:immunology* / Q000382:microbiology*; D005347:Fibroblasts / Q000276:immunology* / Q000382:microbiology*; D005805:Genes, MHC Class I / Q000276:immunology*; D006367:HeLa Cells; D006801:Humans; D061986:MCF-7 Cells