() as a Potential Driver of Molecular Mimicry and Inflammation in Rheumatoid Arthritis.

(; now ) is an infectious agent that causes severe arthritis in swines and shares sequence similarity with residues 261-273 of collagen type 2 (Coll), a possible autoantigen in rheumatoid arthritis (RA). We tested the presence of sequencing 16S ribosomal RNA in crevicular fluid, synovial fluids, and tissues in patients with arthritis (RA and other peripheral arthritides) and in healthy controls. Moreover, we examined the cross-recognition of by Coll-specific T cells in HLA-DRB104 RA patients, by T-cell receptor (TCR) beta chain spectratyping and T-cell phenotyping. DNA was present in 57.4% of the tooth crevicular fluids of RA patients and in 31.6% of controls. Anti- IgM and IgG titers were detectable and correlated with disease duration and the age of the patients. Peripheral blood mononuclear cells (PBMCs) were stimulated with virulence-associated trimeric autotransporter peptide (VtaA10), homologous to human Coll or co-cultured with live . In both conditions, the expanded TCR repertoire overlapped with Coll and led to the production of IL-17. We show that the DNA of an infectious agent (), not previously described as pathogen in humans, is present in most patients with RA and that an peptide is able to activate T cells specific for Coll, likely inducing or maintaining a molecular mimicry mechanism. The cross-reactivity between VtaA10 of a non-human infectious agent and human Coll suggests an involvement in the pathogenesis of RA. This mechanism appears emphasized in predisposed individuals, such as patients with shared epitope.