| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
-Transgenic Mice1
* Division of Allergy, Immunology and Rheumatology, Department of Medicine, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, NY 14203 and Kaleida Health, Buffalo, NY;
Department of Immunology, Sichuan University, Sichuan, China;
Department of Surgery, Kaleida Health, Buffalo, NY 14203;
Department of Hemato-Pathology, M. D. Anderson Cancer Center, Houston, TX 77030;
¶ Immco, Buffalo, NY 14228;
|| Department of Comparative Medicine, State University of New York, Buffalo, NY 14260; and
# Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY 14263
Multiple genetic loci contribute to the development of systemic lupus erythematosus (SLE). In murine models for SLE, various genes on chromosome four have been implicated. IL-14 is a cytokine originally identified as a B cell growth factor. The il14 gene is located on chromosome 4. IL-14
is a cytokine encoded by the plus strand of the IL-14 gene using exons 3–10. The expression of IL-14 is increased in (NZB x NZW)F1 mice. In this study, we produced IL-14-transgenic mice to study the role of IL-14 in the development of autoimmunity. At age 3–9 mo, IL-14-transgenic mice demonstrate increased numbers of B1 cells in the peritoneum, increased serum IgM, IgG, and IgG 2a and show enhanced responses to T-dependent and T-independent Ags compared with littermate controls. At age 9–17 mo, IL-14-transgenic mice develop autoantibodies, sialadenitis, as in Sjögren’s syndrome, and immune complex-mediated nephritis, as in World Health Organization class II SLE nephritis. Between the ages 14–18 mo, 95% of IL-14-transgenic mice developed CD5+ B cell lymphomas, consistent with the lymphomas seen in elderly patients with Sjögren’s syndrome and SLE. These data support a role for IL-14 in the development of both autoimmunity and lymphomagenesis. These studies may provide a genetic link between these often related disorders.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by grants from the Wendt Foundation (to J.L.A.), John R. Oishei Foundation (to J.L.A.), Troup Foundation (to J.L.A.), and Kaleida Health Foundations (to J.L.A.).
2 Address correspondence and reprint requests to Dr. Julian L. Ambrus, Jr., Division of Allergy, Immunology and Rheumatology, School of Medicine and Biomedical Sciences, State University of New York, Room 308 Multiple Lab Building, Buffalo General Hospital, 100 High Street, Buffalo, NY 14203. E-mail address: jambrus{at}buffalo.edu
3 Abbreviations used in this paper: SLE, systemic lupus erythematosus; NZB, New Zealand Black; NZW, New Zealand White; ANA, anti-nuclear Ab; sIg, surface Ig; FISH, fluorescence in situ hybridization; NP, nitrophenyl.
This article has been cited by other articles:
|
|
 |
|
  G. Jiang, Y. Ke, D. Sun, H. Li, M. Ihnen, M. M. Jumblatt, G. Foulks, Y. Wang, Y. Bian, H. J. Kaplan, et al. A New Model of Experimental Autoimmune Keratoconjunctivitis Sicca (KCS) Induced in Lewis Rat by the Autoantigen Klk1b22 Invest. Ophthalmol. Vis. Sci., May 1, 2009; 50(5): 2245 - 2254. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. J. Ford, L. Shen, Y. C. Lin-Lee, L. V. Pham, A. Multani, H.-J. Zhou, A. T. Tamayo, C. Zhang, L. Hawthorn, J. K. Cowell, et al. Development of a murine model for blastoid variant mantle-cell lymphoma Blood, June 1, 2007; 109(11): 4899 - 4906. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
