2018年1月
Induction of short NFATc1/alpha A Isoform Interferes with Peripheral B Cell Differentiation
FRONTIERS IN IMMUNOLOGY
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- 巻
- 9
- 号
- 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
- ID情報
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- DOI : 10.3389/fimmu.2018.00032
- ISSN : 1664-3224
- Web of Science ID : WOS:000423177600001