Yano A, Schwartz R H, Paul W E
Eur J Immunol. 1978 May;8(5):344-7. doi: 10.1002/eji.1830080510.
The activation of T lymphocytes from poly (Glu60Ala30Tyr10)n (GAT)-primed donors by GAT-pulsed nonimmune spleen cells was shown to require identity at the I-1 subregion of the major histocompatibility complex. However, GAT-primed T lymphocytes from (responder x nonresponder) F1 hybrids could only be stimulated to proliferate by GAT bound to high responder or F1 spleen cells but not by GAT bound to spleen cells from the low responder parent. The failure of spleen cells from low responder parental strains to present GAT was shown not to be due to the presence of suppressor cells in either the antigen-presenting or the responding cell populations. These results indicate that control of antigen-presenting cell-T lymphocyte interactions is one site of Ir gene expression.
研究表明,用聚(Glu60Ala30Tyr10)n(GAT)致敏供体的T淋巴细胞被GAT脉冲处理的非免疫脾细胞激活,这需要在主要组织相容性复合体的I-1亚区具有相同性。然而,来自(应答者×非应答者)F1杂种的GAT致敏T淋巴细胞只能被与高应答者或F1脾细胞结合的GAT刺激增殖,而不能被与低应答者亲本脾细胞结合的GAT刺激增殖。低应答者亲本菌株的脾细胞不能呈递GAT,这并非是由于抗原呈递细胞群体或应答细胞群体中存在抑制细胞。这些结果表明,抗原呈递细胞与T淋巴细胞相互作用的控制是Ir基因表达的一个位点。