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jem Home » 1995 Archive » 1 March » 181 (3): 1027
Article

Antifibrillarin autoantibodies present in systemic sclerosis and other connective tissue diseases interact with similar epitopes.

K N Kasturi, A Hatakeyama, H Spiera, C A Bona
K N Kasturi
Department of Microbiology, Mount Sinai School of Medicine, New York 10029-6574.
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A Hatakeyama
Department of Microbiology, Mount Sinai School of Medicine, New York 10029-6574.
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H Spiera
Department of Microbiology, Mount Sinai School of Medicine, New York 10029-6574.
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C A Bona
Department of Microbiology, Mount Sinai School of Medicine, New York 10029-6574.
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DOI: | Published July 1, 1995
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Abstract

Autoantibodies specific against fibrillarin, a 34-kD nucleolar protein associated with U3-snRNP, are present in patients with systemic sclerosis (SSc). To understand the mechanisms involved in the induction of these autoantibodies, we prepared a series of human fibrillarin recombinant proteins covering the entire molecule and analyzed their interaction with the autoantibodies present in various connective tissue diseases. Our results showed that antifibrillarin autoantibodies are present not only in SSc, as previously reported, but also in a variety of other connective tissue diseases. Patients with SSc (58%), mixed connective tissue diseases (60%), CREST syndrome (calcinosis, Raynaud phenomenon, esophageal dismotility, sclerodactyly, and telangiectasia syndrome) (58%), systemic lupus erythematosus (39%), rheumatoid arthritis (60%), and Sjogern's syndrome (84%) showed presence of antifibrillarin autoantibodies. Results obtained from competitive inhibition radioimmunoassay and Western blot analyses with purified recombinant fusion proteins revealed that these autoantibodies react primarily with epitope(s) present in the NH2- (AA 1-80) and COOH-terminal (AA 276-321) domains of fibrillarin. Autoantibodies reacting with internal regions of fibrillarin are less frequent. Analysis of the hydrophilicity profiles of reactive peptides showed presence of three potential antigenic sites in the NH2- and two in the COOH-terminal regions. While a hexapeptide sequence NH2 terminus of fibrillarin is shared with an Epstein-Barr virus-encoded nuclear antigen, the COOH-terminal region shares sequence homology with P40, the capsid protein encoded by herpes virus type 1. Interestingly, these two regions of fibrillarin also contain the most immunodominant sequences, as predicted by surface probability and the Jameson and Wolf antigenic index. These observations suggest that molecular mimicry might play an important role in the induction of antifibrillarin autoantibodies.

© 1995 Rockefeller University Press
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Antifibrillarin autoantibodies present in systemic sclerosis and other connective tissue diseases interact with similar epitopes.
K N Kasturi, A Hatakeyama, H Spiera, C A Bona
Journal of Experimental Medicine Mar 1995, 181 (3) 1027-1036;

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The Journal of Experimental Medicine: 215 (4)

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April 2, 2018
Volume 215, No. 4

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