Table 1.

Common RA-associated microbes.

Microbes	Clinical association	Animal study	Arthritogenic mechanism
Porphyromonas	Clinical association between RA and periodontitis [6–10]. Presence of P. gingivalis DNA in RA patients [17]. Immune responses to P. gingivalis in RA patients [34,35]. Increased anti-P. gingivalis antibodies in subjects with high risk of RA [36].	Immunization with P. gingivalis or P. gingivalis enolase induced or exacerbated arthritis [47–49]. P. gingivalis facilitated destructive arthritis in CIA mice dependent on its peptidylarginine deiminase [51].	Neo-antigen generation [62]. Molecular mimicry [69]. Bystander activation [47,49]. Direct joint damage [88].
Proteus	Clinical association between RA and urinary tract infection [11]. Immune responses to P. mirabilis in RA patients [30–33].		Molecular mimicry [33].
EBV	Clinical association between RA and EBV infection [24]. Presence of EBV DNA and protein in RA patients [21,22]. Immune responses to EBV in RA patients [37,41–43].	EBV induced arthritis in humanized mice [55,56].	Molecular mimicry [70,89]. Superantigen [43,82,83].
Mycoplasma	Presence of DNA [18,19] and glycoglycerophospholipids (GGPL) [29] in RA patients. Immune responses to mycoplasma in RA patients [39,40].	Immunization with mycoplasma arthritidis induced or exacerbated arthritis [46,50,84].	Superantigen [40,50]. Bystander activation [29].