PMC6232707_01
Autoimmune, genetic, and microbial factors associated with Aa-induced early RA. (A) Serial measurements of C-reactive protein (CRP) and anti-cyclic citrullinated peptide (CCP) antibodies. Day 0 marks the diagnosis of Aa endocarditis. Anti-CCP was determined in serum using an automated electrochemiluminescence immunoassay platform (Elecsys, Roche). The dotted line marks the cut-off for anti-CCP antibody positivity (17 U/mL). (B) DNA extracted from patient serum was used to amplify the Aa ltx promoter region by PCR. PCR products of strains Aa HK1651 and Aa SUNY ab75 were used as a reference for JP2 and non-JP2 clones, respectively. The PCR product amplified from patient serum was analyzed by Sanger sequencing. The resulting nucleotide sequence is shown in black. The missing nucleotide sequence corresponding to the 530-bp deletion (Delta530) previously described in Aa JP2 clones is shown in gray. (C) HLA genotype. HLA risk alleles linked to ACPA production and RA are marked in red.
fimmu-09-02352-g0001.jpg
PMC6232707_01_fimmu-09-02352-g0001.jpg
F1
Thereafter, anti-CCP antibody levels started to decline (Figure 1A). At ~1 year follow-up, the patient remained free of joint symptoms, and anti-CCP antibodies and CRP levels had normalized (anti-CCP 13.5 U/mL; CRP 5 mg/L) (Figure 1A).