Coleman D L, Root R K, Ryan J L
J Immunol. 1983 May;130(5):2195-9.
Lymphocytes, activated by lectins or specific antigens, have been shown to enhance macrophage phagocytosis through the elaboration of a heat-labile soluble factor(s). Recent evidence from our laboratory revealed that resident (nonactivated) murine thymocytes and splenic lymphocytes increase peritoneal macrophage glucose metabolism through the elaboration of a heat-stable soluble factor(s). Therefore, we investigated the effect of resident lymphocyte subpopulations on macrophage Fc-dependent phagocytosis. Thioglycollate-elicited and resident peritoneal macrophages from BALB/c mice were cultured in serum-free media with syngeneic resident thymocytes or splenic T lymphocytes. Macrophage Fc-dependent phagocytosis was assayed by measuring the ingestion of 51CrSHEA. After 4 days in vitro, resident thymocytes produced a mean 160 (+/- 31) and 136% (+/- 22) increase in Fc-dependent phagocytosis by thioglycollate-elicited (thio-macrophages) and resident peritoneal macrophages, respectively. Splenic T lymphocytes increased thio-macrophage phagocytosis by 112% (+/- 41) under similar conditions. Macrophage Fc-dependent phagocytosis was increased after 24 hr of co-culture by supernatant derived from resident thymocytes and could be further enhanced by supernatant from Con A-activated thymocytes. Supernatant from guinea pig embryo fibroblasts did not increase macrophage phagocytosis. The soluble factor(s) was produced by resident thymocytes after 24 hr of preculture. This factor was active despite heating at 100 degrees C for 30 min whereas the effect of Con A-activated thymocyte supernatant was heat-labile. The stimulatory effect of resident thymocyte supernatant was not observed when the macrophages and supernatant were cultured in 2% FCS. In contrast to the factor(s) produced by resident thymocytes, the factor(s) in FCS that increased phagocytosis was heat-labile. These data suggest thymocytes and splenic T lymphocytes promote macrophage Fc-dependent phagocytosis in the absence of antigenic or lectin stimulation. This previously unrecognized effect of resident thymocytes is due to a unique heat-stable soluble factor(s) that is concealed in the presence of serum.
已证明，被凝集素或特定抗原激活的淋巴细胞，通过产生一种热不稳定的可溶性因子，可增强巨噬细胞的吞噬作用。我们实验室最近的证据表明，驻留（未激活）的小鼠胸腺细胞和脾淋巴细胞通过产生一种热稳定的可溶性因子，可增加腹腔巨噬细胞的葡萄糖代谢。因此，我们研究了驻留淋巴细胞亚群对巨噬细胞Fc依赖性吞噬作用的影响。将来自BALB/c小鼠的巯基乙酸盐诱导的和驻留的腹腔巨噬细胞，与同基因的驻留胸腺细胞或脾T淋巴细胞一起在无血清培养基中培养。通过测量51CrSHEA的摄取来测定巨噬细胞Fc依赖性吞噬作用。体外培养4天后，驻留胸腺细胞分别使巯基乙酸盐诱导的（硫代巨噬细胞）和驻留腹腔巨噬细胞的Fc依赖性吞噬作用平均增加160%（±31）和136%（±22）。在类似条件下，脾T淋巴细胞使硫代巨噬细胞的吞噬作用增加112%（±41）。驻留胸腺细胞的上清液在共培养24小时后可增加巨噬细胞Fc依赖性吞噬作用，而伴刀豆球蛋白A激活的胸腺细胞的上清液可使其进一步增强。豚鼠胚胎成纤维细胞的上清液不会增加巨噬细胞的吞噬作用。驻留胸腺细胞在预培养24小时后产生可溶性因子。尽管在100℃加热30分钟，该因子仍具有活性，而伴刀豆球蛋白A激活的胸腺细胞上清液的作用是热不稳定的。当巨噬细胞和上清液在2%胎牛血清中培养时，未观察到驻留胸腺细胞上清液的刺激作用。与驻留胸腺细胞产生的因子相反，胎牛血清中增加吞噬作用的因子是热不稳定的。这些数据表明，胸腺细胞和脾T淋巴细胞在无抗原或凝集素刺激的情况下可促进巨噬细胞Fc依赖性吞噬作用。驻留胸腺细胞的这种以前未被认识到的作用是由于一种独特的热稳定可溶性因子，该因子在血清存在时被掩盖。
