Beaman L, Benjamini E, Pappagianis D
Infect Immun. 1983 Mar;39(3):1201-7. doi: 10.1128/iai.39.3.1201-1207.1983.
Previously, it was shown that arthroconidia of Coccidioides immitis appear to inhibit phagosome-lysosome fusion and survive within normal mouse peritoneal macrophages. However, when these macrophages are exposed to antigen-stimulated T lymphocytes from immune mice, activation occurs, leading to enhanced phagosome-lysosome fusion and killing of C. immitis. Results indicate that the activation of macrophages can be effected after incubation with soluble lymphocyte product(s) (lymphokines). The activation of macrophages results if the macrophages are exposed to the lymphokine before, but not after, infection. The results indicate that the lymphocyte population responsible for the elaboration of the lymphokine is phenotypically Lyt1+2- and that activation of macrophages by the lymphokine can occur across H-2 histocompatibility barriers.
先前的研究表明，粗球孢子菌的关节孢子似乎能抑制吞噬体与溶酶体的融合，并在正常小鼠腹膜巨噬细胞内存活。然而，当这些巨噬细胞暴露于来自免疫小鼠的抗原刺激的T淋巴细胞时，巨噬细胞会被激活，导致吞噬体与溶酶体的融合增强，从而杀死粗球孢子菌。结果表明，巨噬细胞与可溶性淋巴细胞产物（淋巴因子）孵育后可被激活。如果巨噬细胞在感染前而非感染后接触淋巴因子，巨噬细胞就会被激活。结果表明，产生淋巴因子的淋巴细胞表型为Lyt1+2-，并且淋巴因子可跨越H-2组织相容性屏障激活巨噬细胞。
