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Chlamydophila pneumoniae downregulates MHC‐class II expression by two cell type‐specific mechanisms
Author(s) -
Peschel Georg,
Kernschmidt Lavinia,
Cirl Christine,
Wantia Nina,
Ertl Tanja,
Dürr Susanne,
Wagner Hermann,
Miethke Thomas,
Rodríguez Nuria
Publication year - 2010
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2010.07114.x
Subject(s) - biology , mhc class i , chlamydophila pneumoniae , mhc class ii , major histocompatibility complex , downregulation and upregulation , microbiology and biotechnology , immunology , antigen , chlamydia , gene , chlamydiaceae , genetics
Summary Chlamydophila pneumoniae was shown to prevent IFNγ‐inducible upregulation of MHC‐class II molecules by secreting chlamydial protease‐like activity factor (CPAF) into the cytosol of those host cells which support the complete bacterial replication cycle. CPAF acts by degrading upstream stimulatory factor 1 (USF‐1). However, in cells like bone marrow‐derived macrophages (BMM), which restrict chlamydial replication, we show that CPAF expression is barely detectable and the expression of USF‐1 is induced upon infection with C. pneumoniae . Nevertheless, the infection still reduced base line and prevented IFNγ‐inducible MHC‐class II expression. Similar results were obtained with heat‐inactivated C. pneumoniae . In contrast, reduction of MHC‐class II molecules was not observed in MyD88‐deficient BMM. Reduction of IFNγ‐inducible MHC‐class II expression by C. pneumoniae in BMM was mediated in part by the MAP‐kinase p38. Infection of murine embryonic fibroblasts (MEF) with C. pneumoniae , which allow chlamydial replication, induced the expression of CPAF and decreased USF‐1 and MHC‐class II expression. Treatment of these cells with heat‐inactivated C. pneumoniae reduced USF‐1 and MHC‐class II expression to a much lower extent. In summary, C. pneumoniae downregulates MHC‐class II expression by two cell type‐specific mechanisms which are either CPAF‐independent and MyD88‐dependent like in BMM or CPAF‐dependent like in MEFs.