論文

査読有り
2010年3月

Reduced T cell expansion by a superantigen as a result of impaired B cell development in mice deficient for the p85 alpha regulatory subunit of PI3K

JOURNAL OF LEUKOCYTE BIOLOGY
  • Yutaka Arimura
  • ,
  • Taichi Ezaki
  • ,
  • Madoka Koyanagi
  • ,
  • Takehiko Uchiyama
  • ,
  • Shigeo Koyasu
  • ,
  • Junji Yagi

87
3
開始ページ
493
終了ページ
500
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1189/jlb.0708440
出版者・発行元
FEDERATION AMER SOC EXP BIOL

PI3K plays crucial roles in the immune system. Mice deficient for p85 alpha, a major regulatory subunit of class IA PI3K, show various defects and alterations in B cells, mast cells, macrophages, and DCs, and peripheral T cells are reportedly normal, at least in vitro. In normal mice, long-term exposure to a SAg, SEA, in vivo induced a high level of the protracted expansion of SEA-reactive V beta 3(+)CD4(+) T cells, whereas the same treatment induced T cell expansion in p85 alpha-deficient mice but to a much lesser extent than in normal mice. However, mixed bone marrow chimera mice, which have normal and p85 alpha-deficient T and B cells, demonstrated equal responses of both T cells following stimulation with a SEA pump. In reciprocal cotransfer experiments of T and B cells from normal and p85 alpha-deficient mice into Rag2-deficient mice, followed by SEA stimulation, p85 alpha-deficient T cells revealed much higher proliferative capacity in the presence of normal B cells than did normal T cells with p85 alpha-deficient B cells. Histologically, a marked B cell reduction was observed in the follicles and MZ of the spleen, and DCs accumulated in the MZ. In addition, p85 alpha-deficient B cells had a low level of MHC class II expression. Collectively, these data suggested that the PI3K p85 alpha subunit alters the SAg presentation capacity of B cells and indirectly modulates the magnitude of the T cell response, which may affect the protection against SEA-containing bacteria. J. Leukoc. Biol. 87: 493-500; 2010.

Web of Science ® 被引用回数 : 3

リンク情報
DOI
https://doi.org/10.1189/jlb.0708440
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/20007249
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000279335700019&DestApp=WOS_CPL

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