The Journal of immunology : official journal of the American Association of Immunologists
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Treatment of mice with 17 beta-estradiol leads to a selective inhibition of natural killer (NK) cell activity as measured by in vitro cytotoxicity against YAC-1 lymphoma and UV-2237 fibrosarcoma target cells. Activation of NK cells by polyinosinic-polycytidylic acid (poly I. C) and Corynebacterium parvum also was impaired in beta-estradiol-treated mice, whereas activation of tumoricidal macrophages was uncompromised. ⋯ Adoptive transfer of normal spleen cells enhanced the NK cell activity and increased the resistance of beta-estradiol-treated mice against hematogenous tumor metastasis. Nude mice treated with beta-estradiol also exhibited a low level of NK cell activity and an enhanced susceptibility to metastasis of allogeneic tumor cells. The potential use of this in vivo model for studies of metastasis of human malignant neoplasms is discussed.
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Intravenous injection of anti-asialo GM1, which has been shown to eliminate natural killer (NK) activity in vitro in the presence of complement, completely abolished NK activity against lymphoma cell line (YAC-1) in spleen cells from athymic nude mice as well as from conventional mice. An immunofluorescence study revealed a decreased number of asialo GM1 positive cells in the spleens of mice injected with anti-asialo GM1 than in those of mice injected with normal rabbit serum. In the nude mice with reduced NK activity, incidence of tumor take and the growth were enhanced when syngeneic (RL male-1), and allogeneic (YAC-1) tumors and human tumors were transplanted subcutaneously. These results strongly suggest that NK cells play an important role in transplanted-tumor growth in vivo.
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Human neutrophils released the granule constituents myeloperoxidase and lysozyme, but not the cytoplasmic enzyme lactic dehydrogenase, when pretreated with cytochalasin B and stimulated with purified human C5a. Prior exposure to C5a before the cytochalasin B, however, abrogated the subsequent secretory process. ⋯ Cytochalasin B effects on neutrophils appear to mimic those of surface binding of soluble stimuli such as C5a and immune complexes. It is suggested that desensitization in concert with surface stimulation may represent an important intracellular mechanism for limiting neutrophil secretion.