Rolstad B, Fossum S, Bazin H, Kimber I, Marshall J, Sparshott S M, Ford W L
Immunology. 1985 Jan;54(1):127-38.
The fate of allogeneic lymphocytes (AO or DA) transferred to non-immune PVG recipients was studied in the light of previous evidence (Heslop & McNeilage, 1983; Rolstad & Ford, 1983) that allogeneic lymphocytes can be rapidly destroyed in certain strain combinations of rats and mice by a mechanism that is distinct from either T-cell mediated immunity or an alloantibody response. AO lymphocytes injected into PVG recipients were discriminated from syngeneic lymphocytes within 15-30 min of i.v. injection, as testified by the excess release of 51Cr into the lymph plasma of the recipient. The following experiments were intended to distinguish between natural antibody and natural killer (NK) cells as the mechanism responsible for the allogeneic lymphocyte cytotoxicity (ALC) displayed by PVG rats. Nude rats treated from birth with anti-mu chain serum and shown to be lacking B and T lymphocytes, as well as being profoundly deficient in immunoglobulin, displayed more aggressive ALC than did control nude rats which, in turn, showed stronger ALC than did euthymic rats. Serum from PVG nude rats exerted no inhibitory or destructive effect on allogeneic lymphocytes in an antibody-dependent cellular cytotoxicity system, an assay of graft-versus-host activity, or when injected into 3-4-week-old PVG rats which had not yet developed ALC. Treatment of nude rats with anti-asialo GM 1 antiserum depressed ALC and NK activity in parallel, thus adding to a wide range of circumstances in which ALC and NK activity are closely correlated. In conclusion, ALC is implemented by a non-adaptive, cell-mediated mechanism independent of immunoglobulin, but the precise identity of the effector cell in the recipients' lymphatic tissues remains to be settled.
根据先前的证据(赫斯洛普和麦克尼尔奇,1983年;罗尔斯塔德和福特,1983年),即同种异体淋巴细胞在大鼠和小鼠的某些品系组合中可通过一种不同于T细胞介导的免疫或同种抗体反应的机制被迅速破坏,研究了转移至未免疫的PVG受体的同种异体淋巴细胞(AO或DA)的命运。静脉注射后15 - 30分钟内,注入PVG受体的AO淋巴细胞就与同基因淋巴细胞区分开来,这可通过向受体淋巴血浆中过量释放51Cr来证明。以下实验旨在区分天然抗体和自然杀伤(NK)细胞,它们是PVG大鼠所表现出的同种异体淋巴细胞细胞毒性(ALC)的负责机制。从出生起就用抗μ链血清处理且显示缺乏B和T淋巴细胞以及免疫球蛋白严重缺乏的裸鼠,其表现出比对照裸鼠更具攻击性的ALC,而对照裸鼠又比正常胸腺大鼠表现出更强的ALC。在抗体依赖性细胞毒性系统、移植物抗宿主活性测定中,或当注入尚未产生ALC的3 - 4周龄PVG大鼠时,PVG裸鼠的血清对同种异体淋巴细胞没有抑制或破坏作用。用抗去唾液酸GM1抗血清处理裸鼠会同时降低ALC和NK活性,这进一步证明了在多种情况下ALC和NK活性密切相关。总之,ALC是由一种不依赖免疫球蛋白的非适应性细胞介导机制实现的,但受体淋巴组织中效应细胞的确切身份仍有待确定。