Wong J F, Elberg S S
J Infect Dis. 1977 Jan;135(1):67-78. doi: 10.1093/infdis/135.1.67.
Resistance to infection with Yersinia pestis was found to depend on whether the macrophage can inactivate and withstand the cytotoxic effects of phagocytized Y. pestis. Serum from mice immunized with antigens of Y. pestis enhanced the resistance of monolayers of normal cultures to the cytotoxic effects of Y. pestis and increased the capacity of peritoneal exudate cells from immune mice to inactivate these bacteria. The enhancing component of the serum was not removed by absorption with heat-killed Y. pestis. Similar enhancement was provided by supernatant fluids of spleen cultures from immunized mice but not by those from unimmunized mice. Pretreatment of spleen cells with rabbit hyperimmune antiserum to mouse brain theta-antigen plus complement caused a reduction in the enhancing capacity of the spleen cell culture fluids. Removal of the glass-adherent cell population from suspensions of primed spleen cells prior to in vitro antigenic stimulation resulted in a loss of activity from the subsequently harvested culture fluids. Thus, the enhancing component of the serum appears to be a product of thymus-derived lymphocytes (T-cells). Furthermore, splenic macrophages seem to be required for the interaction of primed T-cells with heat-killed Y. pestis.
研究发现，对鼠疫耶尔森菌感染的抵抗力取决于巨噬细胞是否能够使吞噬的鼠疫耶尔森菌失活并抵御其细胞毒性作用。用鼠疫耶尔森菌抗原免疫的小鼠血清增强了正常培养单层细胞对鼠疫耶尔森菌细胞毒性作用的抵抗力，并提高了免疫小鼠腹腔渗出细胞使这些细菌失活的能力。血清中的增强成分不会因用热灭活的鼠疫耶尔森菌吸附而去除。免疫小鼠脾脏培养物的上清液也能提供类似的增强作用，但未免疫小鼠的上清液则不能。用兔抗小鼠脑θ抗原超免疫抗血清加补体预处理脾细胞会导致脾细胞培养液的增强能力降低。在体外抗原刺激之前，从致敏脾细胞悬液中去除玻璃黏附细胞群体，会导致随后收获的培养液失去活性。因此，血清中的增强成分似乎是胸腺来源淋巴细胞（T细胞）的产物。此外，致敏T细胞与热灭活的鼠疫耶尔森菌相互作用似乎需要脾巨噬细胞。
