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Post‐translational protein modification in autoimmune epithelitis
Author(s) -
RodriguezRodriguez Mayra,
PérezPérez Maria Elena,
BadilloSoto Adriana,
Bollain y Goytia Juan José,
PachecoTovar Deyanira,
AvalosDíaz Esperanza,
HerreraEsparza Rafael
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.648.10
Subject(s) - citrullination , citrulline , posttranslational modification , autoimmunity , salivary gland , chemistry , arginine , autoantibody , antibody , autoimmune disease , sjögren syndrome , medicine , immunology , enzyme , endocrinology , biochemistry , amino acid
Sjögren's syndrome is an autoimmune epithelitis of salivary and lachrymal glands that results in Sicca syndrome. Citrulline is synthesised by the conversion of ornithine to arginine during urea formation, exists as free citrulline produced by NOS enzymes, and another form produced by post‐translational modification of proteins at arginine residues by peptidylarginine deiminases (PADs), which is important in autoimmunity. We investigate post‐translational reactions in salivary gland biopsies from 24 patients with primary Sjögren's syndrome and 24 controls using immunohistochemistry and a tag‐purified anti‐cyclic citrullinated protein CCP antibody to detect citrullinated peptides, PAD2 also was assessed. The present work demonstrated the weak presence of the PAD2 in some normal salivary ducts (10%), although PAD2 expression was increased considerably in Sjögren's patients. The presence of citrullinated proteins in the salivary tissues of Sjögren's patients strongly supports the in situ post‐translational modification of proteins in this setting. The mutual expression of CCP and PAD2 (70%) suggests that this post‐translational modification is enzyme‐dependent. In conclusion, patients with Sjögren's syndrome expressed the catalytic machinery to produce post‐translational reactions that may result in auto‐antigen triggering. Grant: P/PIFI 2011–32MSU0017H‐06–01