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Autoantibodies to the epidermal growth factor receptor in systemic sclerosis, lupus, and autoimmune mice

STEPHANIE PLANQUE^*, YONG-XIN ZHOU^*, YASUHIRO NISHIYAMA^*, MEENAL SINHA^*, MAUREEN O’CONNOR-MCCOURT, FRANK C. ARNETT^* and SUDHIR PAUL^*1

^* Chemical Immunology and Therapeutics Research Center, Departments of Pathology and Internal Medicine, University of Texas-Houston Medical School, Houston, Texas, USA; and
Biotechnology Research Institute, National Research Council Canada, Montreal, Canada

¹Correspondence: Department of Pathology, MSB 2.250, 6431 Fannin, University of Texas-Houston Medical School, Houston, TX 77030, USA. E-mail: Sudhir.Paul{at}uth.tmc.edu

Autoantibodies to the recombinant extracellular domain of epidermal growth factor receptor (exEGFR) were detected by ELISA in the serum of Fas-defective old MRL/MpJ/lpr and C3H/HeJ/gld mice, but not young mice from these strains, or nonautoimmune young and old BALB/c, MRL/MpJ/++, and C3H/HeJ/MMTV mice. Compared with control human subjects without autoimmune disease, the frequency of exEGFR-binding autoantibodies was increased in scleroderma (systemic sclerosis) patients and to a lesser extent in lupus patients. Phage autoantibodies (Fv fragments) isolated from a lupus library by selection on a linear epitope of EGFR (residues 294–310) displayed the ability to bind exEGFR. Treatment of EGFR-expressing A431 cells with autoantibodies purified by affinity chromatography on immobilized exEGFR resulted in specific staining of the cells. Short-lived but strong inhibition of cellular DNA synthesis was observed in the presence of the autoantibodies. We concluded that autoantibody responses to EGFR hold the potential of fulfilling a pathogenic role in autoimmune disease.—Planque, S., Zhou, Y.-X., Nishiyama, Y., Sinha, M., O’Connor-McCourt, M., Arnett, F.C., Paul, S. Autoantibodies to the epidermal growth factor receptor in systemic sclerosis, lupus, and autoimmune mice.

Key Words: Fas defects • EGFR • antibody library

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