TY - JOUR
T1 - Requirement of CD30 expression on CD4 T cells in the pathogenesis of experimental autoimmune encephalomyelitis
AU - Shinoda, Koji
AU - Sun, Xun
AU - Oyamada, Akiko
AU - Yamada, Hisakata
AU - Kira, Jun ichi
AU - Yoshikai, Yasunobu
N1 - Funding Information:
Jun-ichi Kira is a consultant for Biogen Idec Japan and Medical Review. He has received honoraria from Bayer Healthcare, Mitsubishi Tanabe Pharma, Nobelpharma, Otsuka Pharmaceutical and Medical Review. He is funded by a research grant for Nervous and Mental Disorders from the Ministry of Health, Labour and Welfare, Japan and grants from the Japan Science and Technology Agency and the Ministry of Education, Culture, Sports, Science and Technology, Japan.
Funding Information:
This work was supported by a Grant-in-Aid from the Japan Society for the Promotion of Science , and grants from the Japanese Ministry of Education, Culture, Sports, Science and Technology (Grant number 25670213 , 26293098 ) (Y.Y.), Yakult Bioscience Foundation (Y.Y.) and Takeda Science Foundation (Y.Y.). We thank Kanako Motomura in the Laboratory for Technical Support, Medical Institute of Bioregulation, and Sachiko Koyama in the Department of Neuropathology, Neurological Institute, Kyushu University, for their technical support for the histopathological analysis. We also thank Akiko Yano and Miki Kijima for their technical assistance.
Publisher Copyright:
© 2015 Elsevier B.V.
PY - 2016/2/15
Y1 - 2016/2/15
N2 - CD30, a member of the tumor necrosis factor receptor superfamily, is expressed preferentially by effector or memory helper T cells. Here we show that experimental autoimmune encephalomyelitis (EAE) is ameliorated with markedly reduced induction of antigen-specific Th1 and Th17 cells in CD30 knockout mice. Passive EAE indicated that CD30 on non-hematopoietic parenchymal cell is not required and mixed bone marrow chimera experiments revealed that CD30 signaling on CD4 T cells amplified the development of antigen-specific and encephalitogenic CD4 T cells. Thus, CD30 expression on CD4 T cells is critically involved in the pathogenesis of central nervous system autoimmunity.
AB - CD30, a member of the tumor necrosis factor receptor superfamily, is expressed preferentially by effector or memory helper T cells. Here we show that experimental autoimmune encephalomyelitis (EAE) is ameliorated with markedly reduced induction of antigen-specific Th1 and Th17 cells in CD30 knockout mice. Passive EAE indicated that CD30 on non-hematopoietic parenchymal cell is not required and mixed bone marrow chimera experiments revealed that CD30 signaling on CD4 T cells amplified the development of antigen-specific and encephalitogenic CD4 T cells. Thus, CD30 expression on CD4 T cells is critically involved in the pathogenesis of central nervous system autoimmunity.
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U2 - 10.1016/j.jneuroim.2015.12.005
DO - 10.1016/j.jneuroim.2015.12.005
M3 - Article
C2 - 26857493
AN - SCOPUS:84959387662
SN - 0165-5728
VL - 291
SP - 39
EP - 45
JO - Advances in Neuroimmunology
JF - Advances in Neuroimmunology
ER -