@article{oai:kanazawa-u.repo.nii.ac.jp:00026937,
 author = {Matsushita, Takashi and Fujimoto, Manabu and Hasegawa, Minoru and Komura, Kazuhiro and Takehara, Kazuhiko and Tedder, Thomas F. and Sato, Shinichi},
 issue = {3},
 journal = {American Journal of Pathology},
 month = {Mar},
 note = {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-γ 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 myeiin 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-γ, 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. Copyright © American Society for Investigative Pathology.},
 pages = {812--821},
 title = {Inhibitory Role of CD19 in the Progression of Experimental Autoimmune Encephalomyelitis by Regulating Cytokine Response},
 volume = {168},
 year = {2006}
}