NDLI: Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.

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Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.

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Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Nakayama, Keiichi I. Itsumi, Momoe Yoshikai, Yasunobu Oyamada, Akiko Saiwai, Hirokazu Iwamoto, Yukihide Okada, Seiji Iwakura, Yoichiro Shimoda, Kazuya Ikebe, Hiori Yamada, Hisakata
Description	Country affiliation: Japan Author Affiliation: Oyamada A ( Division of Host Defense, Department of Orthopedic Surgery, Kyushu University, Fukuoka, Japan.)
Abstract	Tyrosine kinase 2 (Tyk2), a member of the JAK family, is involved in IL-12- and IL-23-mediated signaling. In the present study, we examined the roles of Tyk2 in the development of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) by using Tyk2 knockout (KO) mice. In vitro differentiation of Th1 but not Th17 cells was severely impaired in Tyk2 KO CD4 T cells, although Tyk2 KO Th17 cells did not respond to IL-23. Tyk2 KO mice showed complete resistance against EAE with no infiltration of CD4 T cells in the spinal cord. Surprisingly, the number of MOG-specific Th17 cells in the periphery was comparable between KO and wild-type (WT) mice, whereas Th1 cells were greatly reduced in Tyk2 KO mice. Adoptive transfer of MOG-primed WT T cells induced EAE in Tyk2 KO recipients, indicating that Tyk2 in the environment was dispensable for the infiltration of effector T cells into the spinal cord. A reduced but significant number of Tyk2 KO T cells were detected in the spinal cord of mice with EAE, which had been reconstituted with bone marrow cells of WT and KO mice. Furthermore, MOG-immunized Tyk2 KO mice developed EAE after adoptive transfer of MOG-primed WT Th1 cells, which might trigger local inflammation that recruits Th17 cells. Taken together, these results indicate that Tyk2 is critically involved in the pathogenic CD4 T cell responses and thus could be a target molecule for the treatment of autoimmune diseases.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	11
Volume Number	183
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2009-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd4-positive T-lymphocytes Immunology Encephalomyelitis, Autoimmune, Experimental Tyk2 Kinase Adoptive Transfer Animals Cytology Cell Differentiation Cytokines Biosynthesis Genetics Pathology Enzyme-linked Immunosorbent Assay Flow Cytometry Interleukin-17 Mice Mice, Inbred C57bl Mice, Knockout Myelin Proteins Myelin-associated Glycoprotein Myelin-oligodendrocyte Glycoprotein Spinal Cord T-lymphocyte Subsets Metabolism Th1 Cells Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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