Effect of tumor necrosis factor‐α and interferon‐γ on the growth of a human salivary gland cell line
Effect of tumor necrosis factor‐α and interferon‐γ on the growth of a human salivary gland cell line
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肿瘤坏死因子α和干扰素β对人唾液腺细胞系生长的影响
DOI：
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发表时间：
1994
影响因子：
5.6
通讯作者：
J. Atkinson
中科院分区：
文献类型：
--
作者：
A. Wu;R. Kurrasch;J. Katz;P. Fox;B. Baum;J. Atkinson
干扰素-γ（IFN-γ）是活化的T淋巴细胞的产物，肿瘤坏死因子-α（TNF-α）是淋巴细胞和巨噬细胞的产物。这些细胞类型通常存在于继发于慢性感染或自身免疫性疾病的组织损伤部位。本研究的目的是表征TNF-α和IFN-γ对人下颌下腺上皮细胞系（HSG）的影响。IFN-γ导致HSG细胞生长的浓度依赖性降低（6天内> 70%）。相反，单独的TNF-α对这些细胞的生长几乎没有影响。当这些细胞因子组合添加时（20单位/ml TNF-α和1，000单位/ml IFN-γ），存在协同抗增殖作用;未观察到明显的细胞生长。细胞因子诱导的抗增殖作用是可逆的。在细胞生长明显停止3-6天后，去除细胞因子允许完全生长恢复。此外，恢复并表现出与对照细胞相似的生长模式的细胞仍然对细胞因子的抗增殖作用敏感。流式细胞术显示，细胞因子联合作用24 h后，G 0/G1期细胞百分比显著增加。使用IFN-γ受体的抗体完全阻断IFN-γ单独的抗增殖作用以及IFN-γ和TNF-α组合的抗增殖作用。自身免疫性炎症性疾病中组织损伤的假设机制是通过细胞表面标志物如I型细胞间粘附分子（ICAM-1）和组织相容性抗原HLA-DR的上调，这可能加剧炎症过程。用IFN-γ处理HSG细胞，有或没有TNF-α，导致ICAM-1水平增加和HLA-DR表达的获得。这些综合数据表明，单独的IFN-γ可调节炎症过程中涉及的细胞表面标志物的表达，并对HSG细胞生长产生强效但可逆的抑制作用，而HSG细胞生长受TNF-α的存在调节。© 1994 Wiley利斯公司本条目属于美国政府作品，因此在美国属于公有领域。
Interferon‐γ (IFN‐γ) is a product of activated T‐lymphocytes, and tumor necrosis factor‐α (TNF‐α) is a product of both lymphocytes and macrophages. These cell types are often present at sites of tissue damage secondary to chronic infection or autoimmune disease. The purpose of this study was to characterize the effects of TNF‐α and IFN‐γ on a human submandibular gland epithelial cell line (HSG). IFN‐γ caused a concentration‐dependent decrease in HSG cell growth (∼70% in 6 days). Conversely, TNF‐α alone had little effect on the growth of these cells. When these cytokines were added in combination (20 units/ml TNF‐α and 1,000 units/ml of IFN‐γ), there was a synergistic antiproliferative effect; no apparent cell growth was observed. The cytokine‐induced antiproliferative effect was reversible. After the apparent cessation of cell growth for 3–6 days, removal of the cytokines permitted complete growth recovery. Further, cells that recovered and exhibited growth patterns that were similar to control cells remained susceptible to the antiproliferative effects of the cytokines. Flow cytometry revealed that the percentage of cells in G0/G1 with the combination of cytokines was significantly increased by 24 h. The antiproliferative effect of IFN‐γ alone and that of IFN‐γ and TNF‐α in combination were blocked completely using an antibody to the IFN‐γ receptor. A hypothesized mechanism of tissue damage in autoimmune inflammatory disorders is via up‐regulation of cell surface markers such as intercellular adhesion molecule type I (ICAM‐1) and histocompatibility antigen HLA‐DR which can exacerbate the inflammatory process. Treatment of HSG cells with IFN‐γ, with or without TNF‐α, resulted in increased levels of ICAM‐1 and the acquisition of HLA‐DR expression. These aggregate data suggest that IFN‐γ alone can regulate the expression of cell surface markers involved in the inflammatory process as well as cause a potent yet reversible inhibition of HSG cell growth that is modulated by the presence of TNF‐α. © 1994 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.
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肿瘤坏死因子上调人类癌细胞系中γ-干扰素的结合。
DOI：
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发表时间：
1990
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Raitano,AB;Korc,M
通讯作者：
Korc,M
IFN-γ 增强肿瘤坏死因子而非 IL-1 诱导的内皮活化。
DOI：
--
发表时间：
1990
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Doukas,J;Pober,JS
通讯作者：
Pober,JS
干扰素-γ诱导肿瘤坏死因子受体的合成。
DOI：
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发表时间：
1986
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Ruggiero,V;Tavernier,J;Fiers,W;Baglioni,C
通讯作者：
Baglioni,C
干燥综合征唾液腺微环境中细胞粘附分子的表达。
影响因子：
--
作者：
E. William S.T. Clair;John C. Angellilo;Kay H. Singer
通讯作者：
Kay H. Singer