King P D, Sadra A, Han A, Liu X R, Sunder-Plassmann R, Reinherz E L, Dupont B
Immunology Program, Sloan-Kettering Institute for Cancer Research, New York, NY 10021, USA.
Int Immunol. 1996 Nov;8(11):1707-14. doi: 10.1093/intimm/8.11.1707.
Ligation of the CD2 cell surface glycoprotein expressed on T lymphocytes and NK cells induces protein tyrosine phosphorylation and activation of the Src kinases, LCK and FYN. We show here that in Jurkat T leukemia cells and in peripheral blood T cells, CD2 stimulation also leads to tyrosine phosphorylation and activation of the Tec family kinase, EMT/ITK/TSK. Activation of EMT by CD2 was induced by mitogenic pairs of CD2 mAb, certain single CD2 mAb followed by secondary antibody cross-linking, and CD58-bearing sheep red blood cells. With the use of different Jurkat cell mutants it was demonstrated that CD2-mediated activation of EMT required expression of LCK, but not require surface expression of the CD3 zeta chain. Receptor-mediated activation of LCK does not in itself lead to activation of this Tec kinase since induction of LCK by ligation of CD4 or CD5 did not result in activation of EMT. The activation of EMT during CD2 signaling suggests an important role for this kinase in CD2 co-stimulation of T cell responses.
T淋巴细胞和NK细胞表面表达的CD2细胞表面糖蛋白的连接可诱导蛋白酪氨酸磷酸化以及Src激酶LCK和FYN的激活。我们在此表明，在Jurkat T白血病细胞和外周血T细胞中，CD2刺激还会导致Tec家族激酶EMT/ITK/TSK的酪氨酸磷酸化和激活。CD2对EMT的激活是由促有丝分裂的CD2单克隆抗体对、某些单一CD2单克隆抗体继以二抗交联以及携带CD58的绵羊红细胞诱导的。利用不同的Jurkat细胞突变体证明，CD2介导的EMT激活需要LCK的表达，但不需要CD3ζ链的表面表达。受体介导的LCK激活本身并不会导致这种Tec激酶的激活，因为通过CD4或CD5的连接诱导LCK不会导致EMT的激活。CD2信号传导过程中EMT的激活表明该激酶在T细胞反应的CD2共刺激中起重要作用。
