Bolhuis R L, Roozemond R C, van de Griend R J
J Immunol. 1986 Jun 1;136(11):3939-44.
The 50 KD sheep red blood cell antigen receptor CD2 is the earliest T cell differentiation marker and is present on all blood-derived T cells, including natural killer (NK) cells. The CD2 antigen is also known to serve as an important activation site regulating various T cell functions. We report that anti-CD2 monoclonal antibodies (MAb) block MHC-restricted class I- and class II-specific cytolysis by CD2+, CD3+ clones of the relevant target cells, irrespective of whether lysis by these clones is blocked by anti-CD3 or anti-CD8 MAb. Moreover, anti-CD2 MAb (but not anti-CD3 MAb) are able to reduce MHC-nonrestricted, nonspecific cytolysis: a) by CD2+, CD3+ clones of K562 target cells; and b) by CD2+, CD3 NK clones of K562 as well as Daudi cells. Different preparations of anti-CD2 MAb vary in their capacity to inhibit cytolysis. For cloned effector cells, the percent inhibition of lysis by CLB-T11 greater than Lyt-3 MAb, whereas with "fresh" NK cells, the lysis inhibitory ability of Lyt-3 greater than CLB-T11. The antibody-dependent cellular cytotoxicity by "fresh" and cloned NK cells is not inhibited by anti-CD2 MAb. Anti-CD2 MAb also prevent the induction of lysis by cross-linked anti-CD3 MAb, e.g., by CD2+, CD3+ cloned cloned cells against (IgG-FcR+) Daudi cells. Anti-CD2 MAb can also induce cytolysis in some, but not all, CD2+, CD3- NK clones against xenogeneic P815 mouse mastocytoma cells. Anti-CD2 MAb, in combination with lectins (PHA or Con A: pretreatment of effector cells), can also induce cytolytic activity by CD2+, CD3+ clones against Daudi cells. Our data therefore support the concept that the CD2 antigen is an important activation site regulating a wide variety of T cell functions including cytolysis. Whether ligand interaction with the CD2 antigens results in augmentation or inhibition of T cell functions may very well depend on the type of CD2 antigen-ligand interaction, e.g., cross-linked ligand-receptor interaction may, in general, enhance the various T cell functions, whereas noncross-linked ligand-receptor interactions may inhibit such functions, as we and other investigators demonstrated earlier for the CD3/Ti antigen-receptor complex activation site.
50KD的绵羊红细胞抗原受体CD2是最早的T细胞分化标志物，存在于所有血液来源的T细胞上，包括自然杀伤（NK）细胞。已知CD2抗原也是调节各种T细胞功能的重要激活位点。我们报告，抗CD2单克隆抗体（MAb）可阻断相关靶细胞的CD2 +、CD3 +克隆对MHC限制的I类和II类特异性细胞溶解作用，无论这些克隆的细胞溶解作用是否被抗CD3或抗CD8单克隆抗体阻断。此外，抗CD2单克隆抗体（而非抗CD3单克隆抗体）能够降低MHC非限制的非特异性细胞溶解作用：a）K562靶细胞的CD2 +、CD3 +克隆引起的；b）K562以及Daudi细胞的CD2 +、CD3 NK克隆引起的。不同制备的抗CD2单克隆抗体在抑制细胞溶解的能力上有所不同。对于克隆的效应细胞，CLB - T11对细胞溶解的抑制百分比大于Lyt - 3单克隆抗体，而对于“新鲜的”NK细胞，Lyt - 3的细胞溶解抑制能力大于CLB - T11。“新鲜的”和克隆的NK细胞的抗体依赖性细胞毒性不受抗CD2单克隆抗体抑制。抗CD2单克隆抗体还可阻止交联的抗CD3单克隆抗体诱导的细胞溶解作用，例如，CD2 +、CD3 +克隆细胞对（IgG - FcR +）Daudi细胞的作用。抗CD2单克隆抗体也可在一些（但不是全部）CD2 +、CD3 - NK克隆中诱导针对异种P815小鼠肥大细胞瘤细胞的细胞溶解作用。抗CD2单克隆抗体与凝集素（PHA或Con A：效应细胞预处理）联合使用时，也可诱导CD2 +、CD3 +克隆对Daudi细胞的细胞溶解活性。因此，我们的数据支持这样的概念，即CD2抗原是调节包括细胞溶解在内的多种T细胞功能的重要激活位点。配体与CD2抗原的相互作用导致T细胞功能增强还是抑制很可能取决于CD2抗原 - 配体相互作用的类型，例如，交联的配体 - 受体相互作用通常可能增强各种T细胞功能，而非交联的配体 - 受体相互作用可能抑制此类功能，正如我们和其他研究者早期对CD3 / Ti抗原受体复合物激活位点所证明的那样。
