Microbial pathways to subvert host immunity generate citrullinated neoantigens targeted in rheumatoid arthritis |
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| Affiliation: | 1. Department of Bioengineering, University of California Riverside, 900 University Avenue, Riverside, CA, 52512, United States;2. Department of Chemistry, University of California Riverside, 900 University Avenue, Riverside, CA, 52512, United States;1. Center for Theoretical Biological Physics, Rice University, Houston, TX, USA;2. Department of Physics and Astronomy, Rice University, Houston, TX, USA;3. Department of Chemistry, Rice University, Houston, TX, USA;4. Department of Biosciences, Rice University, Houston, TX, USA |
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| Abstract: | The specific association between antibodies to citrullinated proteins and rheumatoid arthritis (RA) has centered interest on understanding why citrullinated proteins become immunogenic in this disease, which is believed to inform the origins of autoimmunity in RA. Since citrullination is a physiologic post-translational modification (PTM), one theory is that conditions promoting abnormal citrullination are initiators of self-reactive immune responses to citrullinated proteins in RA. Foremost candidates that dysregulate the normal balance of citrullination are microbial agents, which can exploit citrullination as an effector mechanism to subvert host antimicrobial activities and maximize their progeny. Here, we will use the host-pathogen interface as a unifying model to link microbe-induced citrullination and the loss of immunological tolerance to citrullinated antigens in RA. |
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