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1
Effects of interferon-gamma and tumour necrosis factor-alpha on the development of cytotoxic T lymphocytes in autologous mixed lymphocyte tumour cultures with human melanoma.γ-干扰素和肿瘤坏死因子-α对人黑色素瘤自体混合淋巴细胞肿瘤培养中细胞毒性T淋巴细胞发育的影响。
Clin Exp Immunol. 1991 Oct;86(1):163-72. doi: 10.1111/j.1365-2249.1991.tb05790.x.
2
Interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha) are necessary in the early stages of induction of CD4 and CD8 cytotoxic T cells by Mycobacterium leprae heat shock protein (hsp) 65 kD.γ干扰素（IFN-γ）和肿瘤坏死因子-α（TNF-α）在麻风分枝杆菌65kD热休克蛋白（hsp）诱导CD4和CD8细胞毒性T细胞的早期阶段是必需的。
Clin Exp Immunol. 1998 Nov;114(2):196-203. doi: 10.1046/j.1365-2249.1998.00702.x.
3
Generation of memory CD4+, CD8+, CD45RO+ and CD16- lymphocytes activated with IL-2, INF-gamma, and TNF-alpha with specific cytotoxicity against autologous cervical cancer cells in a mixed leukocyte-tumour cell culture.在混合白细胞-肿瘤细胞培养中，通过白细胞介素-2、γ干扰素和肿瘤坏死因子-α激活产生具有针对自体宫颈癌细胞特异性细胞毒性的记忆性CD4⁺、CD8⁺、CD45RO⁺和CD16⁻淋巴细胞。
Eur Cytokine Netw. 1995 May-Jun;6(3):195-202.
4
Interferon-alpha (IFN-alpha) stimulates anti-melanoma cytotoxic T lymphocyte (CTL) generation in mixed lymphocyte tumour cultures (MLTC).α干扰素（IFN-α）可在混合淋巴细胞肿瘤培养物（MLTC）中刺激抗黑色素瘤细胞毒性T淋巴细胞（CTL）的生成。
Clin Exp Immunol. 2000 Mar;119(3):412-8. doi: 10.1046/j.1365-2249.2000.01159.x.
5
MHC class-I-restricted auto-tumor-specific CD4+CD8- T-cell clones established from autologous mixed lymphocyte-tumor-cell culture (MLTC).从自体混合淋巴细胞-肿瘤细胞培养（MLTC）中建立的MHC I类限制性自身肿瘤特异性CD4+CD8-T细胞克隆。
Int J Cancer. 1992 Jul 30;51(6):962-7. doi: 10.1002/ijc.2910510621.
6
Increasing infiltration and activation of CD8+ tumor-infiltrating lymphocytes after eliminating immune suppressive granulocyte/macrophage progenitor cells with low doses of interferon gamma plus tumor necrosis factor alpha.在使用低剂量干扰素γ加肿瘤坏死因子α消除免疫抑制性粒细胞/巨噬细胞祖细胞后，CD8 +肿瘤浸润淋巴细胞的浸润和活化增加。
Cancer Immunol Immunother. 1994 Jan;38(1):9-15. doi: 10.1007/BF01517164.
7
Interleukin-12 amplifies the M. leprae hsp65-cytotoxic response in the presence of tumour necrosis factor-alpha and interferon-gamma generating CD56+ effector cells: interleukin-4 downregulates this effect.在肿瘤坏死因子-α和干扰素-γ存在的情况下，白细胞介素-12增强麻风分枝杆菌热休克蛋白65的细胞毒性反应，产生CD56+效应细胞：白细胞介素-4下调这种效应。
Scand J Immunol. 2000 Mar;51(3):262-70. doi: 10.1046/j.1365-3083.2000.00675.x.
8
Interleukin-4 plus tumor necrosis factor alpha augments the antigenicity of melanoma cells.白细胞介素-4加肿瘤坏死因子α增强黑色素瘤细胞的抗原性。
Cancer Immunol Immunother. 1993 Nov;37(6):378-84. doi: 10.1007/BF01526794.
9
Lymphocytes infiltrating ovarian malignant ascites: modulation of IL-2-induced proliferation by IL-4 and of selective increase in CD8+ T cells by TNF-alpha.浸润卵巢恶性腹水的淋巴细胞：白细胞介素-4对白细胞介素-2诱导增殖的调节作用以及肿瘤坏死因子-α对CD8⁺T细胞的选择性增加作用。
Lymphokine Cytokine Res. 1991 Aug;10(4):307-15.
10
In vitro expansion of tumor-specific, HLA-restricted human CD8+ cytolytic T lymphocytes.肿瘤特异性、HLA 限制性人 CD8 + 细胞溶解性 T 淋巴细胞的体外扩增。
Cell Immunol. 1994 Apr 15;155(1):53-61. doi: 10.1006/cimm.1994.1101.

引用本文的文献

1
Mathematical modeling of interleukin-27 induction of anti-tumor T cells response.白细胞介素-27诱导抗肿瘤T细胞反应的数学模型
PLoS One. 2014 Mar 14;9(3):e91844. doi: 10.1371/journal.pone.0091844. eCollection 2014.
2
Preservation of mucosal and systemic adjuvant properties of ISCOMS in the absence of functional interleukin-4 or interferon-gamma.在缺乏功能性白细胞介素-4或干扰素-γ的情况下，免疫刺激复合物（ISCOMS）的黏膜和全身佐剂特性的保留。
Immunology. 1998 Apr;93(4):556-62. doi: 10.1046/j.1365-2567.1998.00469.x.
3
Human recombinant IL-4 decreases the emergence of non-specific cytolytic cells and favours the appearance of memory cells (CD4+CD45RO+) in the IL-2-driven development of cytotoxic T lymphocytes against autologous ovarian tumour cells.在白细胞介素-2驱动的针对自体卵巢肿瘤细胞的细胞毒性T淋巴细胞发育过程中，人重组白细胞介素-4减少了非特异性细胞溶解细胞的出现，并有利于记忆细胞（CD4+CD45RO+）的出现。
Clin Exp Immunol. 1995 Aug;101(2):362-8. doi: 10.1111/j.1365-2249.1995.tb08365.x.

本文引用的文献

1
HLA-DR histocompatibility leukocyte antigens permit cultured human melanoma cells from early but not advanced disease to stimulate autologous lymphocytes.HLA - DR组织相容性白细胞抗原使来自早期而非晚期疾病的培养人黑色素瘤细胞能够刺激自体淋巴细胞。
J Clin Invest. 1984 Jan;73(1):267-71. doi: 10.1172/JCI111201.
2
The role of interleukin-2 (IL-2) in the differentiatin of cytotoxic T cells: the effect of monoclonal anti-IL-2 antibody and absorption with IL-2 dependent T cell lines.白细胞介素-2（IL-2）在细胞毒性T细胞分化中的作用：单克隆抗IL-2抗体的作用及用IL-2依赖型T细胞系进行吸附的效果
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3
Characterization of helper factors distinct from interleukin 2 necessary for the generation of allospecific cytolytic T lymphocytes.鉴定对于同种特异性细胞溶解T淋巴细胞生成所必需的、不同于白细胞介素2的辅助因子。
J Immunol. 1983 Feb;130(2):756-62.
4
Miniaturization of the standard 51Cr release assay for long term follow-up of NK activity of individual mice.用于对个体小鼠自然杀伤细胞活性进行长期跟踪的标准51铬释放试验的小型化。
J Immunol Methods. 1986 Nov 6;93(2):193-200. doi: 10.1016/0022-1759(86)90188-2.
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Cachectin: more than a tumor necrosis factor.恶病质素：不仅仅是一种肿瘤坏死因子。
N Engl J Med. 1987 Feb 12;316(7):379-85. doi: 10.1056/NEJM198702123160705.
6
Inhibition of cytotoxic T cell development by transforming growth factor beta and reversal by recombinant tumor necrosis factor alpha.转化生长因子β对细胞毒性T细胞发育的抑制作用及重组肿瘤坏死因子α的逆转作用。
J Exp Med. 1987 Oct 1;166(4):991-8. doi: 10.1084/jem.166.4.991.
7
Effects of human interleukin 1 and human tumor necrosis factor on human T lymphocyte colony formation.人白细胞介素1和人肿瘤坏死因子对人T淋巴细胞集落形成的影响。
J Clin Invest. 1987 Sep;80(3):772-7. doi: 10.1172/JCI113133.
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Potential uses of interleukin 2 in cancer therapy.白细胞介素2在癌症治疗中的潜在用途。
Immunobiology. 1986 Sep;172(3-5):365-82. doi: 10.1016/S0171-2985(86)80118-8.
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Synergy between interleukin-2 and a second factor in the long-term growth of human T cells.白细胞介素-2与第二种因子在人T细胞长期生长中的协同作用。
Immunology. 1986 Sep;59(1):57-61.
10
Tumor necrosis factor (cachectin) is an endogenous pyrogen and induces production of interleukin 1.肿瘤坏死因子（恶病质素）是一种内源性热原，可诱导白细胞介素1的产生。
J Exp Med. 1986 Jun 1;163(6):1433-50. doi: 10.1084/jem.163.6.1433.

γ-干扰素和肿瘤坏死因子-α对人黑色素瘤自体混合淋巴细胞肿瘤培养中细胞毒性T淋巴细胞发育的影响。

Effects of interferon-gamma and tumour necrosis factor-alpha on the development of cytotoxic T lymphocytes in autologous mixed lymphocyte tumour cultures with human melanoma.

作者信息

Roth A D, Hornicek F J, Gerstner C G, Kirkwood J M

机构信息

Department of Medicine, University of Pittsburgh School of Medicine, PA.

出版信息

Clin Exp Immunol. 1991 Oct;86(1):163-72. doi: 10.1111/j.1365-2249.1991.tb05790.x.

DOI:10.1111/j.1365-2249.1991.tb05790.x
PMID:1833098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1554151/
Abstract

We have studied the influence of tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) on the development of cytotoxic T lymphocytes (CTL) against melanoma in mixed lymphocyte tumour cultures (MLTC). In these MLTC, TNF-alpha at 10(4) U/ml increased the expansion of the CTL up to 10(4)-fold over recombinant IL-2 (rIL-2) alone. IFN-gamma at 10(4) U/ml and combinations of TNF-alpha plus IFN-gamma at 10(2)-10(3) U/ml promoted the proliferation more variably. MLTC generated with rIL-2 showed a predominance of CD8+ cells, while 2 weeks of culture in the presence of IFN-gamma at 10(4) U/ml, or with IFN-gamma and TNF alpha at 1 x 10(2)-10(3) U/ml, favoured the emergence of CD4+ cell populations. The cytotoxic activity of the lymphocytes generated in these MLTC showed a consistent decline of K562 cytotoxic activity following exposure to the combination of IFN-gamma and TNF-alpha. Despite the altered T cell subset distribution with different combinations of cytokines, no consistent alteration in the specific anti-tumour cytotoxicity against melanoma was detected. These results suggest that TNF-alpha and IFN-gamma influence the activation, phenotypic, and functional outcome of MLTC-generated CTL, and may account for the phenotypic variations observed in T cell populations generated in vitro.

摘要

我们研究了肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）在混合淋巴细胞肿瘤培养物（MLTC）中对针对黑色素瘤的细胞毒性T淋巴细胞（CTL）发育的影响。在这些MLTC中，10⁴U/ml的TNF-α使CTL的扩增比单独使用重组白细胞介素-2（rIL-2）增加了高达10⁴倍。10⁴U/ml的IFN-γ以及10²-10³U/ml的TNF-α加IFN-γ组合对增殖的促进作用则更具变化性。用rIL-2产生的MLTC显示CD8⁺细胞占优势，而在10⁴U/ml的IFN-γ存在下培养2周，或与1×10²-10³U/ml的IFN-γ和TNF-α一起培养，则有利于CD4⁺细胞群体的出现。在这些MLTC中产生的淋巴细胞的细胞毒性活性显示，在暴露于IFN-γ和TNF-α的组合后，K562细胞毒性活性持续下降。尽管细胞因子的不同组合改变了T细胞亚群分布，但未检测到针对黑色素瘤的特异性抗肿瘤细胞毒性有一致的改变。这些结果表明，TNF-α和IFN-γ影响MLTC产生的CTL的激活、表型和功能结果，并可能解释了体外产生的T细胞群体中观察到的表型变化。