help button home button Am J Pathol R & D Systems
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Matsushita, T.
Right arrow Articles by Sato, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Matsushita, T.
Right arrow Articles by Sato, S.
(American Journal of Pathology. 2006;168:812-821.)
© 2006 American Society for Investigative Pathology

Inhibitory Role of CD19 in the Progression of Experimental Autoimmune Encephalomyelitis by Regulating Cytokine Response

Takashi Matsushita*, Manabu Fujimoto*, Minoru Hasegawa*, Kazuhiro Komura*, Kazuhiko Takehara*, Thomas F. Tedder{dagger} and Shinichi Sato*{ddagger}

From the Department of Dermatology,* Kanazawa University Graduate School of Medical Science, Kanazawa, Japan; the Department of Immunology,{dagger} Duke University Medical Center, Durham, North Carolina; and the Department of Dermatology,{ddagger} Nagasaki University Graduate School of Biomedical Science, Nagasaki, Japan

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease of the central nerve system that is considered a T helper type 1 (Th1)-mediated autoimmune disease. EAE currently serves as an experimental animal model for multiple sclerosis in human. Cytokines, such as interferon-{gamma} and interleukin-10, play a key role in the development and remission of EAE. Recent studies have also shown a role for B cells in the pathogenesis of EAE. Therefore, we examined the role of CD19, a B cell-specific surface molecule that defines signaling thresholds critical for B-cell responses and autoimmunity, on the development of EAE. Following immunization with myelin oligodendrocyte glycoprotein (MOG) peptide, CD19-deficient (CD19–/–) mice exhibited higher clinical and pathological severity scores of EAE than wild-type mice. The increased severity of EAE in CD19–/– mice was associated with polarized Th1 cytokines in the inflamed central nerve system but not with anti-MOG antibodies in the serum. MOG-primed CD19–/– B cells produced high levels of interferon-{gamma}, and transfer of MOG-primed CD19–/– B cells to wild-type mice worsened the disease. Thus, CD19 modulates the Th1/Th2 cytokine balance in B cells and plays a critical role as a suppressive molecule in the development of EAE.




This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
A. Yoshizaki, Y. Iwata, K. Komura, F. Ogawa, T. Hara, E. Muroi, M. Takenaka, K. Shimizu, M. Hasegawa, M. Fujimoto, et al.
CD19 Regulates Skin and Lung Fibrosis via Toll-Like Receptor Signaling in a Model of Bleomycin-Induced Scleroderma
Am. J. Pathol., June 1, 2008; 172(6): 1650 - 1663.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
C. von Poser-Klein, E. Flechsig, T. Hoffmann, P. Schwarz, H. Harms, R. Bujdoso, A. Aguzzi, and M. A. Klein
Alteration of B-Cell Subsets Enhances Neuroinvasion in Mouse Scrapie Infection
J. Virol., April 1, 2008; 82(7): 3791 - 3795.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
R. Watanabe, M. Fujimoto, N. Ishiura, Y. Kuwano, H. Nakashima, N. Yazawa, H. Okochi, S. Sato, T. F. Tedder, and K. Tamaki
CD19 Expression in B Cells Is Important for Suppression of Contact Hypersensitivity
Am. J. Pathol., August 1, 2007; 171(2): 560 - 570.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Society for Investigative Pathology.