Guo Y J, Lin S C, Wang J H, Bigby M, Sy M S
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106.
Int Immunol. 1994 Feb;6(2):213-21. doi: 10.1093/intimm/6.2.213.
We studied the interactions between CD44 and four different monoclonal anti-CD44 antibodies. All four monoclonal anti-CD44 antibodies studied (P3H9, Bu52, IM.7, and GKW.A3) act in synergy with human anti-CD2 antibodies in stimulating normal human peripheral blood lymphocytes to proliferate. GKW.A3 and IM.7 but not P3H9 or Bu52 inhibited the proliferation of normal human peripheral blood lymphocytes stimulated by anti-CD3. Interestingly, only GKW.A3 and IM.7 stimulated the incorporation of [3H]palmitic acid and palmitoylation of CD44 molecules by normal human peripheral blood lymphocytes. The two monoclonal anti-CD44 antibodies (P3H9 and Bu52) that failed to inhibit anti-CD3 induced proliferation also failed to induce the incorporation of [3H]palmitic acid. More importantly, the inhibitory effects of GKW.A3 were reversed in the presence of cerulenin, an inhibitor of protein palmitoylation. Therefore, palmitoylation of CD44 may interfere with anti-CD3 mediated signaling pathways. These data support the hypothesis that palmitoylation of cell surface receptors may play an active role in receptor and receptor interactions and signal transduction in normal human T lymphocytes.
我们研究了CD44与四种不同的抗CD44单克隆抗体之间的相互作用。所研究的所有四种抗CD44单克隆抗体(P3H9、Bu52、IM.7和GKW.A3)在刺激正常人外周血淋巴细胞增殖方面与人抗CD2抗体协同作用。GKW.A3和IM.7而非P3H9或Bu52抑制抗CD3刺激的正常人外周血淋巴细胞增殖。有趣的是,只有GKW.A3和IM.7刺激正常人外周血淋巴细胞掺入[3H]棕榈酸并使CD44分子棕榈酰化。未能抑制抗CD3诱导的增殖的两种抗CD44单克隆抗体(P3H9和Bu52)也未能诱导[3H]棕榈酸的掺入。更重要的是,在蛋白质棕榈酰化抑制剂浅蓝菌素存在的情况下,GKW.A3的抑制作用被逆转。因此,CD44的棕榈酰化可能干扰抗CD3介导的信号通路。这些数据支持这样的假说,即细胞表面受体的棕榈酰化可能在正常人T淋巴细胞的受体及受体相互作用和信号转导中发挥积极作用。