Human T cell activation. IV. T cell activation and proliferation via the early activation antigen EA 1

S. Nakamura, S. S.J. Sung, J. M. Bjorndahl, S. M. Fu

研究成果: ジャーナルへの寄稿学術誌査読

73 被引用数 (Scopus)

抄録

A new mAb G38 was generated against purified EA 1, an early activation antigen. In immunoprecipitation, it was reactive with the same complex precipitated by the initial anti-EA 1 mAb P8. mAb G38 augmented PMA-induced proliferation of PBMC. It was shown to be mitogenic for purified T cells in collaboration with PMA in a dose-dependent manner. This effect was independent of monocytes and other accessory cells. mAb G38 augmented PMA-induced IL-2-R expression. In conjunction with PMA, it induced IL-2 synthesis and secretion. Its effects on IL-2-R and IL-2 expression were documented at both protein and mRNA levels. Both anti-EA 1 mAbs did not induce Ca2+ influx by themselves in PMA-treated T cells. However, the addition of second anti-mouse Ig antibodies induced readily detectable increases in [Ca2+](i). Ca2+-mediated pathways may be utilized as the transduction signal mechanisms. mAb Leu-23 was shown to be reactive with EA 1. mAb Leu-23 was also mitogenic for T cells in the presence of PMA. These findings provide evidence for a functional role for EA 1 in T cell activation and proliferation.

本文言語英語
ページ(範囲)677-689
ページ数13
ジャーナルJournal of Experimental Medicine
169
3
DOI
出版ステータス出版済み - 1989

!!!All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学

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