PRTN3 and rheumatoid arthritis: However, both anti-CitPG- and anti-CitCII-specific Abs were present at much lower levels in the patients’ sera than those against MCV or CCP3, indicating that autoAbs directed to CitPG and/or CitCII represent a relatively small proportion of the ACPA pool, and may arise as a result of epitope spreading to citrullinated self-proteins during the course of RA [8][44][45].