Arulanandam A R, Koyasu S, Reinherz E L
Laboratory of Immunobiology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115.
J Exp Med. 1991 Apr 1;173(4):859-68. doi: 10.1084/jem.173.4.859.
CD2 subserves both adhesion and signal transduction functions in T cells, thymocytes, and natural killer (NK) cells. In mature T lymphocytes, CD2-mediated signaling function apparently requires surface expression of T cell receptors (TCRs). In contrast, in CD2+ CD3- NK cells and thymocytes, signal transduction through CD2 is TCR independent. To resolve this paradox and characterize TCR-independent triggering mechanisms, we transfected a human CD2 cDNA into a murine mast cell line, C1.MC/57 (Fc epsilon RI+, Fc gamma RII+, Fc gamma RIII+), which is known to produce interleukin 6 (IL-6) as well as release histamine in response to crosslinking of Fc epsilon RI. In the CD2 transfectant, a combination of anti-T11(2) + anti-T11(3) monoclonal antibodies (mAbs) induced a rise in intracellular free calcium [( Ca2+]i), IL-6 production, and histamine release. As expected, no activation was mediated by the same mAbs in C1.MC/57. F(ab)'s fragments of the activatory combination of anti-T11(2) + anti-T11(3) mAbs induced IL-6 in the CD2-transfected mast cells, demonstrating an Fc gamma receptor ectodomain-independent triggering mechanism. In addition, either intact anti-T11(2) or anti-T11(3) IgG alone, which failed to induce [Ca2+]i mobilization in the transfectant, was able to induce IL-6 production. A mAb directed against both Fc gamma RII (previously denoted as Fc gamma RIIb) and Fc gamma RIII (previously denoted as Fc gamma RIIa) inhibits this induction. These results indicate that: (a) Ca2+ mobilization is not essential for IL-6 production; and (b) crosslinking of CD2 and Fc gamma receptors via intact anti-CD2 IgG stimulates IL-6 production. Thus, CD2-mediated IL-6 production occurs by both Fc receptor ectodomain-independent as well as Fc receptor ectodomain-dependent mechanisms in these nonlymphoid cells. Northern blot analysis demonstrates that although the mast cells do not express CD3 zeta or CD3 eta mRNA, they express Fc epsilon RI gamma mRNA. The latter is a known component of Fc gamma RIII as well as Fc epsilon RI, has significant homology to CD3 zeta/eta, and is thought to have a signal transduction function. In these mast cells, CD2 signaling machinery does not require CD3 zeta/eta and may be linked to the Fc epsilon RI gamma subunit. We predict that this subunit or a related structure may confer a TCR-independent signal transduction pathway upon CD2 in CD3- NK cells, thymocytes, and certain B lymphocytes.
CD2在T细胞、胸腺细胞和自然杀伤(NK)细胞中发挥着黏附及信号转导功能。在成熟T淋巴细胞中,CD2介导的信号转导功能显然需要T细胞受体(TCR)的表面表达。相比之下,在CD2⁺CD3⁻NK细胞和胸腺细胞中,通过CD2的信号转导不依赖于TCR。为了解决这一矛盾并阐明不依赖TCR的触发机制,我们将人CD2 cDNA转染到小鼠肥大细胞系C1.MC/57(FcεRI⁺、FcγRII⁺、FcγRIII⁺)中,已知该细胞系在FcεRI交联时会产生白细胞介素6(IL-6)并释放组胺。在CD2转染细胞中,抗T11(2)+抗T11(3)单克隆抗体(mAb)的组合可诱导细胞内游离钙[Ca²⁺]i升高、IL-6产生及组胺释放。正如预期的那样,相同的mAb在C1.MC/57中未介导激活作用。抗T11(2)+抗T11(3) mAb激活组合的F(ab)'片段在CD2转染的肥大细胞中诱导IL-6产生,证明了一种不依赖Fcγ受体胞外域的触发机制。此外,单独的完整抗T11(2)或抗T11(3) IgG虽未能在转染细胞中诱导[Ca²⁺]i动员,但能够诱导IL-6产生。一种针对FcγRII(先前称为FcγRIIb)和FcγRIII(先前称为FcγRIIa)的mAb可抑制这种诱导作用。这些结果表明:(a)Ca²⁺动员对于IL-6产生并非必不可少;(b)通过完整抗CD2 IgG使CD2和Fcγ受体交联可刺激IL-6产生。因此,在这些非淋巴细胞中,CD2介导的IL-6产生通过不依赖Fc受体胞外域以及依赖Fc受体胞外域的机制发生。Northern印迹分析表明,尽管肥大细胞不表达CD3ζ或CD3η mRNA,但它们表达FcεRIγ mRNA。后者是FcγRIII以及FcεRI的已知组成部分,与CD3ζ/η具有显著同源性,并被认为具有信号转导功能。在这些肥大细胞中,CD2信号传导机制不需要CD3ζ/η,可能与FcεRIγ亚基相关。我们预测,该亚基或相关结构可能赋予CD3⁻NK细胞、胸腺细胞和某些B淋巴细胞中CD2一条不依赖TCR的信号转导途径。