Citation
Oyamada, Akiko, et al. "Tyrosine Kinase 2 Plays Critical Roles in the Pathogenic CD4 T Cell Responses for the Development of Experimental Autoimmune Encephalomyelitis." Journal of Immunology (Baltimore, Md. : 1950), vol. 183, no. 11, 2009, pp. 7539-46.
Oyamada A, Ikebe H, Itsumi M, et al. Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis. J Immunol. 2009;183(11):7539-46.
Oyamada, A., Ikebe, H., Itsumi, M., Saiwai, H., Okada, S., Shimoda, K., Iwakura, Y., Nakayama, K. I., Iwamoto, Y., Yoshikai, Y., & Yamada, H. (2009). Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis. Journal of Immunology (Baltimore, Md. : 1950), 183(11), 7539-46. https://doi.org/10.4049/jimmunol.0902740
Oyamada A, et al. Tyrosine Kinase 2 Plays Critical Roles in the Pathogenic CD4 T Cell Responses for the Development of Experimental Autoimmune Encephalomyelitis. J Immunol. 2009 Dec 1;183(11):7539-46. PubMed PMID: 19917699.
TY - JOUR
T1 - Tyrosine kinase 2 plays critical roles in the pathogenic CD4 T cell responses for the development of experimental autoimmune encephalomyelitis.
AU - Oyamada,Akiko,
AU - Ikebe,Hiori,
AU - Itsumi,Momoe,
AU - Saiwai,Hirokazu,
AU - Okada,Seiji,
AU - Shimoda,Kazuya,
AU - Iwakura,Yoichiro,
AU - Nakayama,Keiichi I,
AU - Iwamoto,Yukihide,
AU - Yoshikai,Yasunobu,
AU - Yamada,Hisakata,
Y1 - 2009/11/16/
PY - 2009/11/18/entrez
PY - 2009/11/18/pubmed
PY - 2009/12/23/medline
SP - 7539
EP - 46
JF - Journal of immunology (Baltimore, Md. : 1950)
JO - J Immunol
VL - 183
IS - 11
N2 - 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.
SN - 1550-6606
UR - https://www.unboundmedicine.com/medline/citation/19917699/Tyrosine_kinase_2_plays_critical_roles_in_the_pathogenic_CD4_T_cell_responses_for_the_development_of_experimental_autoimmune_encephalomyelitis_
L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=19917699
DB - PRIME
DP - Unbound Medicine
ER -
