Valdez J C, Mesón O E, Sirena A, de Alderete N G
Mycopathologia. 1987 May;98(2):121-6. doi: 10.1007/BF00437298.
Inoculation of 10(8) C. albicans intraperitoneally into Balb/c mice at given dosage was reported to induce suppression of antigen-specific delayed-type hypersensitivity. Adoptive transfer of spleen cells into normal syngeneic mice pre-treated with Cyclophosphamide confirmed the existence of suppressor cells in mice. Such cells were sensitive to treatment with anti-theta serum and complement, non-adherent to Sephadex G-10. A pretreatment of the mice with Cyclophosphamide eliminated DTH suppression. Treatment with antimacrophage agents via intraperitoneal abrogated suppression only if being effected before inoculation of alive 10(8) Candida albicans. It is concluded that the spleen suppressor cell is a T-lymphocyte whose precursor is Cyclophosphamide-sensitive, requiring the macrophage to be induced.
据报道,以给定剂量将10(8) 白色念珠菌腹腔注射到Balb/c小鼠体内可诱导抗原特异性迟发型超敏反应受到抑制。将脾细胞过继转移到经环磷酰胺预处理的同基因正常小鼠体内,证实小鼠体内存在抑制细胞。此类细胞对抗θ血清和补体治疗敏感,不黏附于葡聚糖凝胶G - 10。用环磷酰胺对小鼠进行预处理可消除迟发型超敏反应抑制。仅在接种活的10(8) 白色念珠菌之前通过腹腔注射抗巨噬细胞剂进行处理,才可消除抑制作用。结论是,脾抑制细胞是一种T淋巴细胞,其前体对环磷酰胺敏感,需要巨噬细胞诱导产生。