Coeliac disease (CD) is becoming a model for understanding the pathogenesis of autoimmune disorders. In CD,
antibodies against
transglutaminase 2 (TG2) and specific residues of
gliadins have been identified. A similar situation is seen in
rheumatoid arthritis (RA) with both
anti-citrullinated protein antibodies (ACPA) and auto-
antibodies against the citrullinating
enzyme,
peptidylarginine deiminase (PAD). Previously, we have suggested that a complex between an
enzyme and its modified substrate constitutes the neoantigen in
autoimmune diseases. Our hypothesis is challenged by findings in patients of primary Sjögren's syndrome (pSS) who do not express ACPA, but who have been reported to carry anti-PAD. The aims of our investigation were to reproduce the study claiming the presence of anti-PAD in pSS and screen for ACPA and
antibodies against TG2 and PAD in pSS (n = 78),
multiple sclerosis (MS) (n = 85) and
Alzheimer's disease (AD) (n = 79) using ELISA. With blood donors (n = 100) as controls, no increased occurrence of
autoantibodies was found among the patient groups tested. Contrary to what has been published previously, patients with pSS do not express anti-PAD. The hypothesis of a complex between an
enzyme and its modified substrate constituting the neoantigen in
autoimmune diseases is still valid. The prevalence of anti-PAD, anti-TG2 and ACPA is comparatively restricted. PAD and TG2 do not seem to be involved directly in autoimmune mechanisms in pSS, MS or AD.