Bentin J, Koutsoukos M, Pierart M, Appelboom T, Ceuppens J L
Division of Rheumatology, Erasmus Hospital, Brussels, Belgium.
Cell Immunol. 1991 Feb;132(2):339-49. doi: 10.1016/0008-8749(91)90032-7.
We investigated the effect of polymorphonuclear neutrophils (PMN) on anti-CD3 mAb (OKT3 and anti-Leu4)-mediated T cell activation. In the absence of monocytes, purified E-rosette-positive cells (further referred to as "T cells") require either solid-phase bound anti-CD3 or the combination of both a high concentration of soluble anti-CD3 and exogenous recombinant interleukin 2 (rIL-2) to proliferate. PMN cannot sustain T cell proliferation with soluble anti-CD3, but they markedly boost proliferation in the presence of soluble anti-CD3 and rIL-2. When PMN were added to T cell cultures stimulated with anti-CD3, this resulted in IL-2 receptor (IL-2R) expression and CD3 modulation. The mechanism of enhancement of anti-CD3-induced IL-2-responsiveness by PMN was further analyzed. A cellular T cell-PMN interaction was found to play a critical role and this was mediated through PMN Fc receptors (FcR). PMN bear two types of low-affinity FcR (FcRII and FcRIII). FcRII is known to bind mIgG1 (e.g., anti-Leu4) and FcRIII binds mIgG2a (e.g., OKT3). FcR involvement was demonstrated by two observations. Anti-FcRII mAb IV.3 inhibited the PMN signal for T cell activation with anti-Leu4. PMN bearing the second variant of FcRII which is unable to bind mIgG1 failed to promote anti-Leu4/IL-2-mediated T cell proliferation. Thus, PMN potentiate T cell responsiveness to IL-2 in the presence of anti-CD3 mAb and this potentiation by PMN requires interaction of anti-CD3 with PMN-FcR.
我们研究了多形核中性粒细胞（PMN）对抗CD3单克隆抗体（OKT3和抗Leu4）介导的T细胞活化的影响。在没有单核细胞的情况下，纯化的E花环阳性细胞（以下简称“T细胞”）需要固相结合的抗CD3或高浓度可溶性抗CD3与外源性重组白细胞介素2（rIL-2）的组合才能增殖。PMN不能通过可溶性抗CD3维持T细胞增殖，但在可溶性抗CD3和rIL-2存在时，它们能显著促进增殖。当将PMN添加到用抗CD3刺激的T细胞培养物中时，这会导致IL-2受体（IL-2R）表达和CD3调节。进一步分析了PMN增强抗CD3诱导的IL-2反应性的机制。发现细胞T细胞与PMN的相互作用起关键作用，这是通过PMN Fc受体（FcR）介导的。PMN带有两种低亲和力FcR（FcRII和FcRIII）。已知FcRII结合mIgG1（例如抗Leu4），FcRIII结合mIgG2a（例如OKT3）。通过两项观察证明了FcR的参与。抗FcRII单克隆抗体IV.3抑制了抗Leu4激活T细胞的PMN信号。携带不能结合mIgG1的FcRII第二种变体的PMN未能促进抗Leu4/IL-2介导的T细胞增殖。因此，在抗CD3单克隆抗体存在下，PMN增强T细胞对IL-2的反应性，并且PMN的这种增强作用需要抗CD3与PMN-FcR相互作用。
