Bagchi A K, Sinha A K
Division of Immunology and Vaccine Development, National Institute of Cholera & Enteric Diseases, P-33, CIT Road, Scheme: XM, Kolkata 700010, India.
J Med Microbiol. 2005 Jul;54(Pt 7):631-637. doi: 10.1099/jmm.0.46014-0.
Antigen-specific T-cell signalling via T-cell antigen receptor stimulation was carried out in BALB/c mice immunized with the 57 kDa major antigenic component of Shigella dysenteriae 1 outer-membrane proteins. In presence of anti-CD3, the 57 kDa antigen was found to increase the level of IL-2 significantly instead of IL-4. IL-2 production in T cells was consistent with an increase in intracellular free Ca(2+) [(Ca(2+))i] concentration. The antigen-specific modulation was observed during T-cell signalling, with enhanced release of [(Ca(2+))i]. IL-2-receptor stimulation via IL-2 did not significantly induce the release of IL-2 with consistent intracellular Ca(2+) production. Furthermore, the protein tyrosine kinase was activated during anti-CD3 stimulation, which up-regulated the phosphatidylinositol kinase of p85-mediated serine kinase protein kinase-C of p70. Phosphoinositide-specific kinases are regulated by the phosphorylation of tyrosine kinase through the activation of the T-cell antigen receptor. The above findings indicate that phosphotidylinositol-3 kinase-mediated signals are up-regulated through [(Ca(2+))i], which is essential for Th1-type responses.
在用痢疾志贺氏菌1型外膜蛋白的57 kDa主要抗原成分免疫的BALB/c小鼠中,通过T细胞抗原受体刺激进行抗原特异性T细胞信号传导。在抗CD3存在的情况下,发现57 kDa抗原显著增加IL-2水平而非IL-4水平。T细胞中IL-2的产生与细胞内游离Ca(2+) [(Ca(2+))i]浓度的增加一致。在T细胞信号传导过程中观察到抗原特异性调节,[(Ca(2+))i]的释放增强。通过IL-2刺激IL-2受体并未显著诱导IL-2的释放,细胞内Ca(2+)产生一致。此外,在抗CD3刺激过程中蛋白酪氨酸激酶被激活,这上调了p85介导的丝氨酸激酶蛋白激酶C的p70的磷脂酰肌醇激酶。磷酸肌醇特异性激酶通过T细胞抗原受体的激活由酪氨酸激酶的磷酸化调节。上述发现表明磷脂酰肌醇-3激酶介导的信号通过[(Ca(2+))i]上调,这对Th1型反应至关重要。