Silagi S, Dutkowski R, Schaefer A
Department of Obstetrics and Gynecology, Cornell University Medical College, New York, NY 10021.
Anticancer Res. 1988 Nov-Dec;8(6):1265-9.
Localized treatment with recombinant human interleukin-2 (rIL-2) +/- recombinant murine interferon-gamma (rIFN-gamma) results in regression of early B16 melanomas in normal C57BL/6 (B6) mice, but not in syngeneic beige mice, which have defective natural killer (NK) cells. Injection of antibodies to asialo GM1 (a-AGM1) or Thy1 abolishes the tymoricidal effects of rIL-1 +/- rIFN-gamma. Thus, cells activated by these cytokines must be either NK-like cells that are AGM1+ Thy1+, or NK-like cells (AGM1+) cooperating with T lymphocytes (Thy1+), since either antibody (a-AGM1 or a-Thy1) independently abrogates the in vivo antitumor effect.
用重组人白细胞介素-2（rIL-2）+/-重组鼠干扰素-γ（rIFN-γ）进行局部治疗可使正常C57BL/6（B6）小鼠的早期B16黑色素瘤消退，但同基因的米色小鼠则不然，这些米色小鼠的自然杀伤（NK）细胞存在缺陷。注射抗唾液酸化GM1（a-AGM1）或Thy1抗体可消除rIL-1+/-rIFN-γ的杀肿瘤作用。因此，被这些细胞因子激活的细胞必定是a-AGM1+Thy1+的NK样细胞，或者是与T淋巴细胞（Thy1+）协同作用的NK样细胞（a-AGM1+），因为任何一种抗体（a-AGM1或a-Thy1）均可独立消除体内抗肿瘤作用。
