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Comparative effects of cytokines and cytokine combinations on complement component C3 secretion by HepG2 cells 总被引:4,自引:0,他引:4
The mechanisms that control complement protein synthesis are incompletely understood. Recent evidence suggests that cytokines are involved in the regulation of hepatic synthesis of circulating complement components. Therefore, we compared the effects of human recombinant IL-1alpha, IL-1beta, IL-6, IFN-gamma, and TNF-alpha individually or in combination, on HepG2 secretion of complement component C3, the major opsonic protein of the complement system. HepG2 cells were incubated with each cytokine alone and with various combinations of the cytokines. At 24, 48, 72, and 96 h of incubation, the C3 and albumin secreted by the HepG2 cells were quantified by a sandwich ELISA. IL-1alpha and IFN-gamma significantly enhanced C3 secretion by the cells (P<0.02 vs. control cells). IL-1beta when combined with either IL-6 or IFN-gamma also increased C3 secretion (P<0.03 vs. control cells). The stimulatory effect on HepG2 cells by the IL-1beta/IL-6 combination was synergistic. With the exception of IL-1alpha, which increased albumin secretion, HepG2 secretion of albumin was not affected by incubation with individual cytokines or the cytokine combinations. Therefore, IL-1alpha, IFN-gamma, and the combination of IL-1beta with IL-6 or IFN-gamma specifically enhanced C3 secretion by HepG2 cells. The greatest magnitude of C3 secretion was induced by the combination of IL-1beta and IL-6. 相似文献
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How cells respond to interferons revisited: from early history to current complexity 总被引:3,自引:0,他引:3
Stark GR 《Cytokine & growth factor reviews》2007,18(5-6):419-423
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Paul J. Hertzog Seung Y. Hwang Ismail Kola 《Molecular reproduction and development》1994,39(2):226-232
There now appears to be evidence to support the view that the type I IFNs are naturally produced negative regulators of growth that also modify cell differentiation. Consistent with this, it appears that the ability to produce and respond to IFN is suppressed in early embryonic development when cell proliferation and differentiation are essential. In the later stages of fetal development, IFN production is de-repressed, and cells show increased sensitivity to IFN, which may be important in regulating cell proliferation and/or differentiation processes or the interaction between fetal and maternal tissues. Interestingly, the IFN system can also be suppressed in disease states such as the development of tumours or in the establishment of a (chronic) viral infection. Therefore, understanding the developmental regulation of the IFN system may be important to understanding and controlling the IFN system in disease. More extensive studies of the developmental stage and tissue-specific expression of type I IFNs and their receptors are necessary, as well as more direct in vivo experiments to further elucidate the role of the IFN system in reproduction and development. © 1994 Wiley-Liss, Inc. 相似文献
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Abstract: It is recognized that tumor necrosis factor-α (TNF-α), a pleiotropic cytokine, influences hormone secretion and transmitter release from central neurons. To examine the role of TNF-α as a modulator of autonomic function of the PNS, we measured [3 H]norepinephrine ([3 H]NE) secretion evoked by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), a nicotinic agonist, in cultures from neonatal rat superior cervical ganglia (SCG). We found that (1) DMPP-evoked [3 H]NE secretion was enhanced in SCG mixed cultures treated for 48 h with recombinant human TNF-α (rhTNF-α) plus rat interferon-γ (IFN-γ) but not in cultures treated with either cytokine alone; (2) an increase in [3 H]NE secretion was also observed in mixed cultures treated with recombinant murine TNF-α (rmTNF-α) alone; and (3) the presence of nonneuronal cells or soluble factors released by them was required for the effect of these cytokines on secretion. Electrophysiologic experiments revealed an increase in nicotinic receptor current density in neurons from mixed cultures treated with rhTNF-α plus IFN-γ or with rmTNF-α when compared with control cultures. We conclude that prolonged exposure to rhTNF-α plus IFN-γ or rmTNF-α regulates nicotinic responses in SCG cultures via a soluble factor or factors secreted by nonneuronal cells. 相似文献
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There were seven workshops that primarily concerned the biological effects of the interferons and the other cytokines. These were: Workshop 6, The refractory state in the reponse to interferons (IFNs) and antibodies in treated patients; Workshop 7, IFNs, multiple sclerosis, and the nervous system; Workshop 9, Viral inhibition of the response to IFNs and other cytokines; Workshop 10, Cell growth inhibition by IFNs and other cytokines; Workshop 12, Cytokines and cell death; Workshop 13, Interactions between cytokines; and, Workshop 14, Cytokine gene therapy. Summaries of each of these sessions follow. 相似文献
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