MISC

2004年7月

Impairment of B cell receptor-mediated Ca2+ influx, activation of mitogen-activated protein kinases and growth inhibition in CD72-deficient BAL-17 cells

INTERNATIONAL IMMUNOLOGY
  • M Ogimoto
  • ,
  • G Ichinowatari
  • ,
  • N Watanabe
  • ,
  • N Tada
  • ,
  • K Mizuno
  • ,
  • H Yakura

16
7
開始ページ
971
終了ページ
982
記述言語
英語
掲載種別
DOI
10.1093/intimm/dxh100
出版者・発行元
OXFORD UNIV PRESS

CD72 is a 45 kDa B cell-specific type II transmembrane protein of the C-type lectin superfamily. It was originally defined as a receptor-like molecule that regulates B cell activation and differentiation; however, its precise function remains unclear since more recent functional analyses, including a gene targeting study, suggest that CD72 may serve as a negative or a positive regulator of B cell signaling. In the present study, we analyzed the cell-autonomous function of CD72 in B cell receptor (BCR) signaling using CD72-deficient cells generated from mature BAL-17 cells. We found that BCR-mediated phosphorylation of CD19, Btk, Vav and phospholipase Cgamma2 and association of CD19 with phosphatidylinositol-3 kinase were impaired in CD72-deficient cells. Inositol trisphosphate synthesis was normally induced initially but ablated at 1 min of stimulation in CD72-deficient cells. In the event, Ca2+ release from intracellular stores remained intact, though influx of extracellular Ca2+ was severely impaired in CD72-deficient cells. Furthermore, BCR-evoked activation of mitogen-activated protein kinases (MAPKs), extracellular signal-regulated kinase and c-Jun NH2-terminal kinase, and growth inhibition in BAL-17 cells were blocked in the absence of CD72. Significantly, these effects were largely reversed by re-expression of CD72. Thus, CD72 appears to exert a positive effect on BCR signaling pathways leading to Ca2+ influx and MAPK activation, which in turn may determine the fate of BAL-17 cells.

Web of Science ® 被引用回数 : 11

リンク情報
DOI
https://doi.org/10.1093/intimm/dxh100
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000222121700009&DestApp=WOS_CPL

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