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Autoimmunity to deltaNp63alpha in Chronic Ulcerative Stomatitis

L.W. Solomon1,*, M.E. Neiders2, M.G. Zwick2,3, K.L. Kirkwood4, and V. Kumar3,5

1 Department of Oral and Maxillofacial Pathology, School of Dental Medicine, Tufts University, DHS-646A, One Kneeland Street, Boston, MA 02111-1527, USA;
2 Department of Oral Diagnostic Sciences, School of Dental Medicine, University at Buffalo, SUNY, Buffalo, NY, USA;
3 IMMCO Diagnostics, Inc., Buffalo, NY, USA;
4 Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, MI; and
5 Departments of Microbiology and Dermatology, University at Buffalo, SUNY, Buffalo, NY, USA


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Figure. All CUS sera studied have antibodies to {Delta}Np63{alpha}, and 52% have serum IgA. Western transfers of deltaNp63alpha protein, produced by in vitro transcription/translation, were immunoblotted with sera. (A,B) Results from 21 different CUS patient sera (numbered lanes) and the mAb 4A4. [Lane #/serum #, as follows: 1/572, 2/3069, 3/4045, 4/4787, 5/4792, 6/9264, 7/8985, 8/9035, 9/8051, 10/5742, 11/622, 12/8216, 13/S.J., 14/180, 15/1631, 16/10808, 17/512; 18E47; 19/E67; 20/E81; 21/IM0017.] (A) All of the sera have antibodies to deltaNp63alpha protein. (B) Eleven of the 21 sera have IgA antibodies detected with goat anti-human IgA secondary antibody. (C) Control sera tested were 16 diagnostic samples from patients with clinical dermatologic or rheumatic conditions. None of the controls had antibodies to deltaNp63alpha protein. mAb = monoclonal antibody, MW = molecular-weight marker.

 





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