Nakashima M, Janiszewska M, Steplewski Z, Watanabe T, Schuchter L, Koprowski H
Department of Molecular Immunology, Kyushu University, Fukuoka, Japan.
Hybridoma. 1994 Jun;13(3):241-6. doi: 10.1089/hyb.1994.13.241.
The effects of human recombinant interleukin-4 (rIL-4) on metastatic melanoma (lymph node)-derived T lymphocytes cultured with human recombinant interleukin-2 (rIL-2) were studied. Lymphocytes isolated from melanoma-invaded lymph nodes were cultured in media with rIL-2 in the presence (MB-2,4) or absence (MB-2) or rIL-4 for up to 48 days. A majority of lymphocytes grown in both cultures were CD3+ T lymphocytes. Addition of rIL-4 to the rIL-2 culture abrogated the growth of the CD3-, CD56+ cell population [natural killer (NK) cell], which were present in culture with rIL-2 alone. Lymph-node-derived T lymphocytes that had expanded under MB-2,4 conditions lysed only autologous melanoma cells and they maintained the autologous-specific cytolytic activity during the entire culture period. They did not lyse K562, Daudi, or allogeneic target cells. Monoclonal antibodies (MAbs) against CD3 molecules and MHC class I molecules but not MHC class II molecules inhibited the specific lytic functions of T lymphocytes under MB-2,4 culture conditions. Collectively, these data indicate that in lymphocyte culture derived from melanoma-invaded lymph nodes, rIL-4 inhibits the rIL-2-dependent proliferation of NK cells and antigen nonspecific killer T lymphocytes and also effectively abrogates the rIL-2-induced NK and lymphokine-activated killer (LAK) activities.
研究了人重组白细胞介素-4(rIL-4)对用人重组白细胞介素-2(rIL-2)培养的转移性黑色素瘤(淋巴结)来源的T淋巴细胞的影响。从黑色素瘤浸润的淋巴结中分离出的淋巴细胞在含有rIL-2的培养基中培养,分别添加rIL-4(MB-2,4组)或不添加rIL-4(MB-2组),培养长达48天。两种培养物中生长的大多数淋巴细胞都是CD3 + T淋巴细胞。在rIL-2培养物中添加rIL-4可消除CD3 - 、CD56 +细胞群体(自然杀伤细胞)的生长,该细胞群体仅在单独使用rIL-2培养时存在。在MB-2,4条件下扩增的淋巴结来源的T淋巴细胞仅裂解自体黑色素瘤细胞,并且在整个培养期间保持自体特异性细胞溶解活性。它们不裂解K562、Daudi或同种异体靶细胞。针对CD3分子和MHC I类分子而非MHC II类分子的单克隆抗体在MB-2,4培养条件下抑制T淋巴细胞的特异性裂解功能。总的来说,这些数据表明,在黑色素瘤浸润的淋巴结来源的淋巴细胞培养中,rIL-4抑制rIL-2依赖的NK细胞和抗原非特异性杀伤性T淋巴细胞的增殖,并且还有效消除rIL-2诱导的NK和淋巴因子激活的杀伤细胞(LAK)活性。