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Inhibitory role of CD19 in the progression of experimental autoimmune encephalomyelitis by regulating cytokine response.
Am J Pathol. 2006 Mar; 168(3):812-21.AJ

Abstract

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.

Authors+Show Affiliations

Department of Dermatology, Kanazawa University Graduate School of Medical Science, 13-1 Takaramachi, Kanazawa, Ishikawa 920-8641, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16507897

Citation

Matsushita, Takashi, et al. "Inhibitory Role of CD19 in the Progression of Experimental Autoimmune Encephalomyelitis By Regulating Cytokine Response." The American Journal of Pathology, vol. 168, no. 3, 2006, pp. 812-21.
Matsushita T, Fujimoto M, Hasegawa M, et al. Inhibitory role of CD19 in the progression of experimental autoimmune encephalomyelitis by regulating cytokine response. Am J Pathol. 2006;168(3):812-21.
Matsushita, T., Fujimoto, M., Hasegawa, M., Komura, K., Takehara, K., Tedder, T. F., & Sato, S. (2006). Inhibitory role of CD19 in the progression of experimental autoimmune encephalomyelitis by regulating cytokine response. The American Journal of Pathology, 168(3), 812-21.
Matsushita T, et al. Inhibitory Role of CD19 in the Progression of Experimental Autoimmune Encephalomyelitis By Regulating Cytokine Response. Am J Pathol. 2006;168(3):812-21. PubMed PMID: 16507897.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibitory role of CD19 in the progression of experimental autoimmune encephalomyelitis by regulating cytokine response. AU - Matsushita,Takashi, AU - Fujimoto,Manabu, AU - Hasegawa,Minoru, AU - Komura,Kazuhiro, AU - Takehara,Kazuhiko, AU - Tedder,Thomas F, AU - Sato,Shinichi, PY - 2006/3/2/pubmed PY - 2006/4/20/medline PY - 2006/3/2/entrez SP - 812 EP - 21 JF - The American journal of pathology JO - Am. J. Pathol. VL - 168 IS - 3 N2 - 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. SN - 0002-9440 UR - https://www.unboundmedicine.com/medline/citation/16507897/Inhibitory_role_of_CD19_in_the_progression_of_experimental_autoimmune_encephalomyelitis_by_regulating_cytokine_response_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0002-9440(10)62142-6 DB - PRIME DP - Unbound Medicine ER -