Over‐expression of TATA binding protein (TBP) and p53 and autoantibodies to these antigens are features of systemic sclerosis, systemic lupus erythematosus and overlap syndromes | Zendy

Chauhan R. | Zendy; Handa R. | Zendy; Das T. P. | Zendy; Pati U. | Zendy

Open Access

Over‐expression of TATA binding protein (TBP) and p53 and autoantibodies to these antigens are features of systemic sclerosis, systemic lupus erythematosus and overlap syndromes

Author(s) -

Chauhan R.,

Handa R.,

Das T. P.,

Pati U.

Publication year - 2004

Publication title -

clinical & experimental immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.329

H-Index - 135

eISSN - 1365-2249

pISSN - 0009-9104

DOI - 10.1111/j.1365-2249.2004.02463.x

Subject(s) - autoantibody , antigen , immunology , medicine , antibody , connective tissue disease , immune system , titer , mixed connective tissue disease , autoimmunity , extractable nuclear antigens , lupus erythematosus , autoimmune disease , systemic disease , immunopathology , anti nuclear antibody

Summary The aim of this study was to determine the expression levels of p53 and TATA binding protein (TBP) and the presence of autoantibodies to these antigens in Asian Indian patients with systemic sclerosis (SSc), overlap syndromes (OS) and systemic lupus erythematosus (SLE). Fifty patients with SSc, 20 with OS, including mixed connective tissue diseases (MCTD), 20 with SLE, 10 disease controls (DC) and 25 controls (C) were studied. The over‐expression of p53 and TBP antigen was determined quantitatively by sandwich enzyme‐linked immunosorbent assay (ELISA), varies between four‐ and sevenfold higher in patients with SSc, OS and SLE, in comparison to DC and C. The expressed protein antigens were not present as free antigens but as immune‐complexes. Autoantibodies to p53 were detected by ELISA in 78% subjects with SSc, 100% with OS and 80% with SLE. Autoantibodies to TBP were observed in 28% patients with SSc, 25% with OS and 15% with SLE. In comparison to healthy controls, the titre of antibodies to p53 was significantly higher in patients with SSc ( P = 0·00001) than the patients with OS ( P = 0·00279) and SLE ( P = 0·00289), whereas the titre of antibodies to TBP was higher in patients with OS ( P = 0·00185) than the SLE ( P = 0·00673) and the SSc ( P = 0·00986) patients. Autoantibodies to p53 and TBP were detected in all these patients and the levels of these two autoantibodies showed weak negative correlation with each other. We propose that the over‐expression of these antigens might be due to hyperactive regulatory regions in the p53 and TBP gene.

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