Rahman S M, Pu M Y, Yi H, Ohkusu K, Kato M, Isobe K, Taguchi R, Ikezawa H, Nakashima I
Department of Immunology, Nagoya University School of Medicine, Japan.
Infect Immun. 1995 Jan;63(1):259-63. doi: 10.1128/iai.63.1.259-263.1995.
Phosphatidylinositol-specific phospholipase C (PIPLC) from Bacillus thuringiensis, which cleaves phosphatidylinositol or glycosylphosphatidylinositol on the external cell surface to generate a second messenger for intracellular signal transduction (S. Rahman et al., FEBS Lett. 303:193-196, 1992), was found to preferentially promote the generation of alloantigen-specific cytotoxic T lymphocytes in mixed leukocyte culture. PIPLC affected an early stage of cytotoxic T-lymphocyte activation in culture, and there was no evidence of any soluble cellular mediators of this PIPLC action. PIPLC neither enhanced overall cell proliferation nor noticeably promoted interleukin-2 and -4 production in mixed leukocyte culture. The relative population size of Ly-2+ T cells was increased, however, in a late mixed leukocyte culture with PIPLC. In addition, PIPLC enhanced an anti-CD3 monoclonal antibody-induced early increase in [Ca2+]i. These results suggest a new parasite (bacterium)-oriented mechanism for enhancing antigen-driven host cytotoxic T-lymphocyte immunity which does not include promotion of interleukin-2 production.
苏云金芽孢杆菌的磷脂酰肌醇特异性磷脂酶C(PIPLC)可切割细胞外表面的磷脂酰肌醇或糖基磷脂酰肌醇,以产生用于细胞内信号转导的第二信使(S. Rahman等人,《欧洲生物化学学会联合会快报》303:193 - 196,1992年),研究发现它在混合淋巴细胞培养中能优先促进同种异体抗原特异性细胞毒性T淋巴细胞的产生。PIPLC影响培养中细胞毒性T淋巴细胞激活的早期阶段,且没有证据表明存在这种PIPLC作用的任何可溶性细胞介质。在混合淋巴细胞培养中,PIPLC既没有增强总体细胞增殖,也没有显著促进白细胞介素-2和-4的产生。然而,在含有PIPLC的晚期混合淋巴细胞培养中,Ly-2 + T细胞的相对群体大小增加了。此外,PIPLC增强了抗CD3单克隆抗体诱导的细胞内钙离子浓度([Ca2+]i)早期升高。这些结果提示了一种新的以寄生虫(细菌)为导向的增强抗原驱动的宿主细胞毒性T淋巴细胞免疫的机制,该机制不包括促进白细胞介素-2的产生。