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開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Regulation of microglial homeostasis through cell-cell interaction signal

  • P2-208
  • 橋本 美穂 / Miho Hashimoto:1 林 由里子 / Yuriko Hayashi:1 草苅 伸也 / Shinya Kusakari:2 小谷 武徳 / Takenori Kotani:3 村田 陽二 / Yoji Murata:3 的崎 尚 / Takashi Matozaki:3 大西 浩史 / Hiroshi Ohnishi:1 
  • 1:群馬大院・保健・生体情報 / Dept Lab Sci, Gunma Univ Grad Sch Health Sci, Gunma, Japan 2:群馬大・生体調節研・バイオシグナル / Lab Biosig Sci, Inst Mol Cell Reg, Gunma Univ, Gunma, Japan 3:神戸大院・医・シグナル統合 / Div Mol Cell Signal, Dept Biochem Mol Biol, Kobe Univ Grad Sch Med, Kobe, Japan 

It has been known that an increase of brain immune cells expressing CD11c, which is a dendric cell (DC) marker, occurs commonly in the aged and inflamed brain. However, the pathological or physiological significance of CD11c-positive cells in such states of the brain is not fully understood. Signal regulatory protein α (SIRP α ), an immunoglobulin superfamily (IgSF) membrane protein that is predominantly expressed in DC or macrophages in the immune system, mediates cell-cell communication signal by interacting with CD47, another IgSF membrane protein. In the central nervous system, both SIRP α and CD47 are predominantly expressed in neurons. SIRP α is also expressed in microglia, while roles of the CD47-SIRP α signal in regulation of microglial cell functions remain unclear. We found that genetic ablation of SIRP α induced an increase in the number of cells that expressed CD11c in the brain of SIRP α knockout mice. These brain CD11c-positive (bCD11c+) cells expressed microglial marker proteins, CD11b and Iba-1. In addition, the expression level of CD45, a marker protein for hematopoietic cells, was intermediate or low in the bCD11c+ cells. These results suggest that the bCD11c+ cells belong to a subpopulation of brain-resident microglia. These bCD11c+ microglia also expressed CD14 or Dectin-1, cell surface receptors characteristically expressed on cells that contribute to induction of the innate immune response. An increase in the number of the bCD11c+ microglia was also observed in CD47 KO mice, suggesting that lack of the interaction between CD47 and SIRP α resulted in the same phenotype. Although the cell types that are mainly involved in the CD47-SIRP α signal and thus control the number of bCD11c+ microglia remains to be defined, intercellular interaction mediated by CD47 and SIRP α is critical to maintain homeostasis of brain microglia.

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