Requirement of CD30 expression on CD4 T cells in the pathogenesis of experimental autoimmune encephalomyelitis

Koji Shinoda; Xun Sun; Akiko Oyamada; Hisakata Yamada; Jun-Ichi Kira; Yasunobu Yoshikai

doi:10.1016/j.jneuroim.2015.12.005

Requirement of CD30 expression on CD4 T cells in the pathogenesis of experimental autoimmune encephalomyelitis

J Neuroimmunol. 2016 Feb 15:291:39-45. doi: 10.1016/j.jneuroim.2015.12.005. Epub 2015 Dec 11.

Authors

Koji Shinoda¹, Xun Sun², Akiko Oyamada³, Hisakata Yamada³, Jun-Ichi Kira⁴, Yasunobu Yoshikai⁵

Affiliations

¹ Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan; Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
² Department of Immunology, China Medical University, Shenyang 110001, China.
³ Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.
⁴ Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
⁵ Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan. Electronic address: yoshikai@bioreg.kyushu-u.ac.jp.

PMID: 26857493
DOI: 10.1016/j.jneuroim.2015.12.005

Abstract

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.

Keywords: CD30; CD30 ligand; Experimental autoimmune encephalomyelitis; Multiple sclerosis.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
CD4-Positive T-Lymphocytes / drug effects
CD4-Positive T-Lymphocytes / metabolism*
Cytokines / metabolism
Disease Models, Animal
Dose-Response Relationship, Drug
Encephalomyelitis, Autoimmune, Experimental / chemically induced
Encephalomyelitis, Autoimmune, Experimental / immunology
Encephalomyelitis, Autoimmune, Experimental / pathology*
Flow Cytometry
Ki-1 Antigen / deficiency*
Ki-1 Antigen / genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Myelin-Oligodendrocyte Glycoprotein
Peptide Fragments
Spinal Cord / pathology*
Th1 Cells / immunology
Th17 Cells / immunology
Thymidine / metabolism
Time Factors
Tritium / metabolism

Substances

Cytokines
Ki-1 Antigen
Myelin-Oligodendrocyte Glycoprotein
Peptide Fragments
myelin oligodendrocyte glycoprotein (35-55)
Tritium
Thymidine