NDLI: Nitric oxide and KLF4 protein epigenetically modify class II transactivator to repress major histocompatibility complex II expression during Mycobacterium bovis bacillus Calmette-Guerin infection.

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Nitric oxide and KLF4 protein epigenetically modify class II transactivator to repress major histocompatibility complex II expression during Mycobacterium bovis bacillus Calmette-Guerin infection.

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Nitric oxide and KLF4 protein epigenetically modify class II transactivator to repress major histocompatibility complex II expression during Mycobacterium bovis bacillus Calmette-Guerin infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Holla, Sahana Sinha, Akhauri Yash Alagesan, Senthil Kumar Balaji, Kithiganahalli Narayanaswamy Ghorpade, Devram Sampat
Description	Author Affiliation: Ghorpade DS ( Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, India.)
Abstract	Pathogenic mycobacteria employ several immune evasion strategies such as inhibition of class II transactivator (CIITA) and MHC-II expression, to survive and persist in host macrophages. However, precise roles for specific signaling components executing down-regulation of CIITA/MHC-II have not been adequately addressed. Here, we demonstrate that Mycobacterium bovis bacillus Calmette-Guérin (BCG)-mediated TLR2 signaling-induced iNOS/NO expression is obligatory for the suppression of IFN-Î³-induced CIITA/MHC-II functions. Significantly, NOTCH/PKC/MAPK-triggered signaling cross-talk was found critical for iNOS/NO production. NO responsive recruitment of a bifunctional transcription factor, KLF4, to the promoter of CIITA during M. bovis BCG infection of macrophages was essential to orchestrate the epigenetic modifications mediated by histone methyltransferase EZH2 or miR-150 and thus calibrate CIITA/MHC-II expression. NO-dependent KLF4 regulated the processing and presentation of ovalbumin by infected macrophages to reactive T cells. Altogether, our study delineates a novel role for iNOS/NO/KLF4 in dictating the mycobacterial capacity to inhibit CIITA/MHC-II-mediated antigen presentation by infected macrophages and thereby elude immune surveillance.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	28
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-07-12
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Histocompatibility Antigens Class II Immunology Kruppel-Like Transcription Factors Nitric Oxide Nuclear Proteins Trans-Activators Tuberculosis Animals Cell Line Cells, Cultured Epigenesis, Genetic Gene Expression Drug Effects Genetics Metabolism Host-Pathogen Interactions Immunoblotting Interferon-gamma Pharmacology Macrophages Microbiology Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout MicroRNAs Microscopy, Confocal Mycobacterium Bovis Physiology Nitric Oxide Synthase Type II Polycomb Repressive Complex 2 RNA Interference Reverse Transcriptase Polymerase Chain Reaction Veterinary Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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