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2012/07/31
Rong-Rong Songa, Huan-Renb, Wei Sunc, Xu-Wenb, Cheng-bin Zhaod, Jing Qud, Feng Liand, Ben-ning Zhangb, e, Chan Lif, Hong Zhangf, H
iroyuki Abeg, Kazuhiro Tadab, e, Yun-long Qid, e,
a. Department of Neurology, The Fourth Affiliated Hospital of Harbin Medical University, China
b .Department of Immunology, Harbin Medical University, China
c. Department of Oncology, The Second Affiliated Hospital of Harbin Medical University, China
d. Department of Orthopedics, The Fourth Affiliated Hospital of Harbin Medical University, Heilongjiang 150086, China
e. Department of Immunology, The Institute of Medical Oncology, Japan
f. Department of Neuropathology, Medical Research Institute, Tokyo Medical and Dental University, Japan
g. Kudan Clinic, The Institute of Medical Oncology, Japan
【Abstract】
NK1.1+ natural killer (NK)-T cells reactive to CD1 appear to be involved in spontaneous autoimmune disease, but their role in induced
autoi mmune disease remains unclear. While we previously reported a regulatory role of NK cells in experimental autoimmune
encephalomyelitis (EAE), we demonstrate here that NK-T cells would also play a pivotal role in the control of EAE. C57BL/6 (B6) mice
selectively depleted for NK-T cells were generated by antibody-depended protocols or knocking out TCRJα281 gene. Regardless of the
method for NK-T cell deletion, these NK-T depleted mice developed unusually early onset of EAE (5–8 days after challenge) after
immunization with an encephalitogenic peptide myelin oligodendrocyte glycoprotein (MOG)35–55. The early EAE onset was associated
with early induction of T helper cell type 1 (Th1) cells and marked elevation of Th1 cytokines in the serum. It was of note that,
although the NK-T deficient mice spontaneously recovered from EAE, mice selectively depleted for NK cells developed a later onset
of non-remitting EAE. These data establish differential roles played by NK-T and NK cells in the protection against EAE.
• 국제개별화의료학회(지)
Volume 1, Issue 1, July 2012, Pages 18–24
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