Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (13)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Ohkouchi, K.
Right arrow Articles by Shimizu, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ohkouchi, K.
Right arrow Articles by Shimizu, M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 11, No. 10, 1635-1640, October 1999
© 1999 Japanese Society for Immunology

Anti-elongation factor-1{alpha} autoantibody in adult atopic dermatitis patients

Kumiko Ohkouchi, Hitoshi Mizutani, Minoru Tanaka1, Machiko Takahashi, Kunio Nakashima1 and Masayuki Shimizu

Departments of Dermatology and
1 Biochemistry, Faculty of Medicine, Mie University, 2-174 Edobashi, Tsu, Mie 514-8507, Japan

Correspondence to: H. Mizutani

Adult atopic dermatitis (AD) patients develop severe facial lesions, which sometimes distribute in sun-exposed areas similar to the rash of systemic lupus erythematosus. To declare autoimmunity in the pathogenesis of AD, we investigated serum antinuclear antibody (ANA) in 256 adult AD patients and identified its ligands. A high titer of ANA was found in 31.3% of AD patients and 75% of the ANA showed a homogenous pattern. Sixty-five percent of ANA+ sera reacted to a 52 kDa protein (p52) in HeLa cell immunoblots. By screening the HeLa cell cDNA expression library with anti-p52 sera, a clearly positive clone was isolated. The sequence of this cDNA was identical to human elongation factor (hEF)-1{alpha}. The eluate of IgG bound to hEF-1{alpha}–glutathione S-transferase (GST) fusion protein recognized a band at 52 kDa in a HeLa cell immunoblot, and stained Hep-2 cell nuclei and cytoplasma as reported in hEF-1{alpha} distribution. The anti-p52 AD sera recognized the hEF-1{alpha}–GST fusion protein. The anti-hEF-1{alpha} antibody-positive AD patients were characterized by higher facial involvement and lower white blood cell counts compared with antibody-negative patients. The present results suggest the possible involvement of autoimmunity in the pathogenesis of adult AD.

Keywords: allergen, allergy, autoimmunity, erythematosus, exanthema

Transmitting editor: M. Miyasaka


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
ASH Education BookHome page
N. Berliner, M. Horwitz, and T. P. Loughran Jr.
Congenital and Acquired Neutropenia
Hematology, January 1, 2004; 2004(1): 63 - 79.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
H. J. Ditzel, Y. Masaki, H. Nielsen, L. Farnaes, and D. R. Burton
Cloning and expression of a novel human antibody-antigen pair associated with Felty's syndrome
PNAS, August 1, 2000; 97(16): 9234 - 9239.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
J. K. Sandberg, L. Franksson, J. Sundback, J. Michaelsson, M. Petersson, A. Achour, R. P. A. Wallin, N. E. Sherman, T. Bergman, H. Jornvall, et al.
T Cell Tolerance Based on Avidity Thresholds Rather Than Complete Deletion Allows Maintenance of Maximal Repertoire Diversity
J. Immunol., July 1, 2000; 165(1): 25 - 33.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.