論文

2018年1月

Induction of short NFATc1/alpha A Isoform Interferes with Peripheral B Cell Differentiation

FRONTIERS IN IMMUNOLOGY
  • Khalid Muhammad
  • ,
  • Ronald Rudolf
  • ,
  • Duong Anh Thuy Pham
  • ,
  • Stefan Klein-Hessling
  • ,
  • Katsuyoshi Takata
  • ,
  • Nobuko Matsushita
  • ,
  • Volker Ellenrieder
  • ,
  • Eisaku Kondo
  • ,
  • Edgar Serfling

9
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3389/fimmu.2018.00032
出版者・発行元
FRONTIERS MEDIA SA

In lymphocytes, immune receptor signals induce the rapid nuclear translocation of preformed cytosolic NFAT proteins. Along with co-stimulatory signals, persistent immune receptor signals lead to high levels of NFATc1/alpha A, a short NFATc1 isoform, in effector lymphocytes. Whereas NFATc1 is not expressed in plasma cells, in germinal centers numerous centrocytic B cells express nuclear NFATc1/alpha A. When overexpressed in chicken DT40 B cells or murine WEHI 231 B cells, NFATc1/alpha A suppressed their cell death induced by B cell receptor signals and affected the expression of genes controlling the germinal center reaction and plasma cell formation. Among those is the Prdm1 gene encoding Blimp-1, a key factor of plasma cell formation. By binding to a regulatory DNA element within exon 1 of the Prdm1 gene, NFATc1/alpha A suppresses Blimp-1 expression. Since expression of a constitutive active version of NFATc1/alpha A interfered with Prdm1 RNA expression, LPS-mediated differentiation of splenic B cells to plasmablasts in vitro and reduced immunoglobulin production in vivo, one may conclude that NFATc1/alpha A plays an important role in controlling plasmablast/plasma cell formation.

リンク情報
DOI
https://doi.org/10.3389/fimmu.2018.00032
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000423177600001&DestApp=WOS_CPL
ID情報
  • DOI : 10.3389/fimmu.2018.00032
  • ISSN : 1664-3224
  • Web of Science ID : WOS:000423177600001

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