Tomonari K, Spencer S
Transplantation Biology Section, MRC Clinical Research Centre, Harrow, UK.
Int Immunol. 1990;2(12):1189-94. doi: 10.1093/intimm/2.12.1189.
Functions of the CD8 molecule were examined to determine whether CD8 is merely a ligand-binding molecule and/or is involved in signal transduction. Using KT112 (anti-CD8 beta), CD8 was demonstrated to transduce an activation signal leading to cytotoxicity. Conformational changes of the CD8 molecule might be responsible for the activation, because (i) KT15 (anti-monomorphic CD8 alpha), but not antibodies specific for polymorphic CD8 alpha determinants, abrogated KT112 (anti-CD8 beta)-induced cytotoxicity without blocking the binding of KT112, whilst (ii) KT112 (anti-CD8 beta) inhibited KT15 (anti-monomorphic CD8 alpha)-mediated augmentation of proliferation triggered by a V beta 11-specific antibody without blocking the binding of KT15.
研究了CD8分子的功能,以确定CD8是否仅仅是一种配体结合分子和/或是否参与信号转导。使用KT112(抗CD8β),证明CD8可转导导致细胞毒性的激活信号。CD8分子的构象变化可能是激活的原因,因为:(i)KT15(抗单态性CD8α),而非针对多态性CD8α决定簇的特异性抗体,可消除KT112(抗CD8β)诱导的细胞毒性,而不阻断KT112的结合;同时(ii)KT112(抗CD8β)抑制KT15(抗单态性CD8α)介导的由Vβ11特异性抗体触发的增殖增强,而不阻断KT15的结合。