Beretta A, Persson U, Ramos T, Möller G
Scand J Immunol. 1982 Sep;16(3):181-9. doi: 10.1111/j.1365-3083.1982.tb00713.x.
The effects of concanavalin A (Con A) on the effector phase of specific and nonspecific cytotoxicity were studied. The addition of the lectin to the cytotoxicity assay resulted in inhibition of specific cytotoxicity and induced the lysis of nonspecific targets only when the lectin was added after the target cells. Preincubation of the effector cells with the ligand strongly inhibited specific cytotoxicity and did not induce nonspecific cytotoxicity. However, preincubation of the target cells with Con A before addition to the assay had no effect on the specific lysis and strongly facilitated the lysis of nonspecific targets. The inhibitory effect was not due to the agglutinating property of the lectin, since another agglutinogenic and non-mitogenic lectin (Helix pomatia) did not inhibit cytotoxicity. Induction of effector-to-effector killing seemed unlikely, since the addition of Con A to 51Cr-labelled effector cells did not significantly enhance the release of isotope. The inhibitory effect could be reversed by a subsequent incubation of the Con A-treated effectors with alpha-methyl-d-mannoside. We suggest that Con A inhibits specific alloreactive cytotoxicity by blocking the antigen-binding receptors of T cells and induces nonspecific cytotoxicity by already activated cytotoxic T lymphocytes (CTLs) by binding to the major histocompatibility complex (MHC) antigens of the targets and creating structures mimicking allogenic MHC products that will be recognized by CTLs via the antigen-binding receptors.
研究了伴刀豆球蛋白A(Con A)对特异性和非特异性细胞毒性效应阶段的影响。在细胞毒性测定中加入凝集素会抑制特异性细胞毒性,并且只有在靶细胞之后加入凝集素时才会诱导非特异性靶细胞的裂解。效应细胞与配体预孵育会强烈抑制特异性细胞毒性,且不会诱导非特异性细胞毒性。然而,在加入测定之前用Con A对靶细胞进行预孵育对特异性裂解没有影响,并且会强烈促进非特异性靶细胞的裂解。这种抑制作用并非由于凝集素的凝集特性,因为另一种具有凝集原性且无丝裂原性的凝集素(苹果蜗牛凝集素)不会抑制细胞毒性。效应细胞对效应细胞杀伤的诱导似乎不太可能,因为向51Cr标记的效应细胞中加入Con A并未显著增强同位素的释放。Con A处理过的效应细胞随后与α-甲基-D-甘露糖苷孵育可逆转这种抑制作用。我们认为,Con A通过阻断T细胞的抗原结合受体来抑制特异性同种异体反应性细胞毒性,并通过与靶细胞的主要组织相容性复合体(MHC)抗原结合,形成模仿同种异体MHC产物的结构,从而诱导已激活的细胞毒性T淋巴细胞(CTL)产生非特异性细胞毒性,这些结构将被CTL通过抗原结合受体识别。