Claesson M H, Dissing S, Tscherning T, Geisler C
Laboratory of Experimental Immunology, Panum Institute, University of Copenhagen, Denmark.
Immunology. 1993 Mar;78(3):444-8.
We have studied activation-induced changes in intracellular calcium [Ca2+]i, interleukin-2 (IL-2) secretion, and clonal abortion of the human leukaemic T-cell line Jurkat and three T-cell receptor (TcR)/CD3 receptor negative clones deficient for the TcR alpha, TcR beta and CD3 gamma chains respectively, as well as three transfectant clones reconstituted with the appropriate TcR/CD3 cDNA. For activation, the cells were exposed to anti-TcR/CD3, anti-CD2 and anti-major histocompatibility complex (anti-MHC) class I monoclonal antibodies (mAb) respectively. Cellular activation by these mAb leading to an increased IL-2 secretion was preceded by a rise in [Ca2+]i and was relatively dependent on the expression of the a TcR/CD3 complex. In contrast, anti-MHC class I mAb-induced clonal abortion in Jurkat T cells may occur without previous fluctuations in [Ca2+]i and appeared to be independent of TcR/CD3 expression. The present observation suggest the existence of different secondary messenger systems operating in Jurkat cells following activation via the TcR/CD3, CD2 and the MHC class I pathways, respectively.
我们研究了激活诱导的人白血病T细胞系Jurkat以及分别缺乏T细胞受体(TcR)α、TcRβ和CD3γ链的三个TcR/CD3受体阴性克隆,以及三个用适当的TcR/CD3 cDNA重建的转染克隆细胞内钙[Ca2+]i、白细胞介素-2(IL-2)分泌和克隆流产的变化。为了激活细胞,分别将细胞暴露于抗TcR/CD3、抗CD2和抗主要组织相容性复合体(抗MHC)I类单克隆抗体(mAb)。这些mAb导致IL-2分泌增加的细胞激活之前是[Ca2+]i的升高,并且相对依赖于αTcR/CD3复合体的表达。相反,抗MHC I类mAb诱导的Jurkat T细胞克隆流产可能在[Ca2+]i没有先前波动的情况下发生,并且似乎独立于TcR/CD3表达。目前的观察结果表明,在通过TcR/CD3、CD2和MHC I类途径激活后,Jurkat细胞中分别存在不同的第二信使系统。