Hambor J E, Tykocinski M L, Kaplan D R
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106.
J Exp Med. 1988 Oct 1;168(4):1237-45. doi: 10.1084/jem.168.4.1237.
An experimental approach for defining the function of CD8 has been developed by linking anti-sense RNA mutagenesis and T cell cloning technologies. We have transfected an anti-sense CD8 episomal expression vector into a CD8+ nontransformed human T cell clone that is specific for the human class I alloantigen HLA-B35. Expression of CD8 on this T cell clone, JH.ARL.1, was selectively and efficiently inhibited. Stimulation of this CD8- variant with specific alloantigen resulted in a marked loss of a number of functional responses, including cytotoxicity, proliferation, IL-2 secretion, and IL-2-R expression. However, these same functional responses could be elicited with stimuli that do not require antigen recognition to activate the T cell (anti-CD3 mAbs, PHA). The results of our study support the hypothesis that CD8 is required for recognition of class I MHC alloantigens that results in activation of T cell functional responses.
通过将反义RNA诱变技术与T细胞克隆技术相结合，已开发出一种用于确定CD8功能的实验方法。我们已将反义CD8附加型表达载体转染到一个针对人类I类同种异体抗原HLA - B35的CD8 + 未转化人类T细胞克隆中。该T细胞克隆JH.ARL.1上CD8的表达被选择性且高效地抑制。用特异性同种异体抗原刺激这个CD8缺陷变体导致许多功能反应明显丧失，包括细胞毒性、增殖、IL - 2分泌和IL - 2 - R表达。然而，这些相同的功能反应可以由不需要抗原识别来激活T细胞的刺激（抗CD3单克隆抗体、PHA）引发。我们的研究结果支持这样的假设，即识别导致T细胞功能反应激活的I类MHC同种异体抗原需要CD8。
