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Interleukin-12 (IL-12) and IL-23 induction of substance p synthesis in murine T cells and macrophages is subject to IL-10 and transforming growth factor beta regulation.白细胞介素-12（IL-12）和IL-23诱导小鼠T细胞和巨噬细胞中P物质合成受IL-10和转化生长因子β调控。
Infect Immun. 2008 Aug;76(8):3651-6. doi: 10.1128/IAI.00358-08. Epub 2008 May 27.
2
IL-12 induction of mRNA encoding substance P in murine macrophages from the spleen and sites of inflammation.白细胞介素-12诱导来自脾脏和炎症部位的小鼠巨噬细胞中编码P物质的信使核糖核酸。
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3
IL-10 and TGF-beta redundantly protect against severe liver injury and mortality during acute schistosomiasis.白细胞介素-10和转化生长因子-β在急性血吸虫病期间对严重肝损伤和死亡具有冗余性保护作用。
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Arginase I suppresses IL-12/IL-23p40-driven intestinal inflammation during acute schistosomiasis.精氨酸酶 I 抑制急性血吸虫病期间 IL-12/IL-23p40 驱动的肠道炎症。
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Transforming growth factor (TGF)-beta1-producing regulatory T cells induce Smad-mediated interleukin 10 secretion that facilitates coordinated immunoregulatory activity and amelioration of TGF-beta1-mediated fibrosis.产生转化生长因子（TGF）-β1的调节性T细胞诱导Smad介导的白细胞介素10分泌，这有助于协调免疫调节活性并改善TGF-β1介导的纤维化。
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Mycobacterium avium infection of macrophages results in progressive suppression of interleukin-12 production in vitro and in vivo.鸟分枝杆菌感染巨噬细胞会导致体外和体内白细胞介素-12生成的逐渐抑制。
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Curcumin modulation of IFN-beta and IL-12 signalling and cytokine induction in human T cells.姜黄素对人T细胞中IFN-β和IL-12信号传导及细胞因子诱导的调节作用
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Downregulation of interleukin-12 (IL-12) responsiveness in human T cells by transforming growth factor-beta: relationship with IL-12 signaling.转化生长因子-β对人T细胞中白细胞介素-12（IL-12）反应性的下调作用：与IL-12信号传导的关系
Blood. 1999 Mar 1;93(5):1448-55.
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The production of IFN-gamma by IL-12/IL-18-activated macrophages requires STAT4 signaling and is inhibited by IL-4.IL-12/IL-18激活的巨噬细胞产生干扰素-γ需要STAT4信号传导，并受到IL-4的抑制。
J Immunol. 2001 Mar 1;166(5):3075-82. doi: 10.4049/jimmunol.166.5.3075.

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A Novel Murine Model of Radiation Keratopathy.一种新型的放射性角膜病变小鼠模型。
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Enhanced expressions of neurodegeneration-associated factors, UPS impairment, and excess Aβ accumulation in the hippocampus of mice with persistent cerebral toxocariasis.持久性脑弓蛔虫病小鼠海马中与神经退行性变相关的因子、UPS 损伤和过量 Aβ 积累的增强表达。
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本文引用的文献

1
STAT3 and NF-kappaB signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice.在自发性关节炎动物模型白细胞介素-1受体拮抗剂缺陷小鼠中，信号转导及转录激活因子3（STAT3）和核因子κB（NF-κB）信号通路是白细胞介素-23介导白细胞介素-17产生所必需的。
J Immunol. 2006 May 1;176(9):5652-61. doi: 10.4049/jimmunol.176.9.5652.
2
New IL-12-family members: IL-23 and IL-27, cytokines with divergent functions.新型白细胞介素-12家族成员：白细胞介素-23和白细胞介素-27，功能各异的细胞因子。
Nat Rev Immunol. 2005 Jul;5(7):521-31. doi: 10.1038/nri1648.
3
IL-12 induction of mRNA encoding substance P in murine macrophages from the spleen and sites of inflammation.白细胞介素-12诱导来自脾脏和炎症部位的小鼠巨噬细胞中编码P物质的信使核糖核酸。
J Immunol. 2005 Apr 1;174(7):3906-11. doi: 10.4049/jimmunol.174.7.3906.
4
Signaling by IL-12 and IL-23 and the immunoregulatory roles of STAT4.白细胞介素-12和白细胞介素-23信号传导以及信号转导和转录激活因子4的免疫调节作用。
Immunol Rev. 2004 Dec;202:139-56. doi: 10.1111/j.0105-2896.2004.00211.x.
5
IL-12 and IL-23: master regulators of innate and adaptive immunity.白细胞介素-12和白细胞介素-23：固有免疫和适应性免疫的主要调节因子。
Immunol Rev. 2004 Dec;202:96-105. doi: 10.1111/j.0105-2896.2004.00214.x.
6
Cutting edge: hemokinin has substance P-like function and expression in inflammation.前沿：血激肽在炎症中具有类似P物质的功能和表达。
J Immunol. 2004 Jun 1;172(11):6528-32. doi: 10.4049/jimmunol.172.11.6528.
7
The role of substance P, hemokinin and their receptor in governing mucosal inflammation and granulomatous responses.P物质、血激肽及其受体在调控黏膜炎症和肉芽肿反应中的作用。
Front Biosci. 2004 May 1;9:1936-43. doi: 10.2741/1375.
8
Substance P regulates Th1-type colitis in IL-10 knockout mice.P物质调节白细胞介素-10基因敲除小鼠的1型结肠炎。
J Immunol. 2003 Oct 1;171(7):3762-7. doi: 10.4049/jimmunol.171.7.3762.
9
IL-18 and IL-12 signal through the NF-kappa B pathway to induce NK-1R expression on T cells.白细胞介素-18和白细胞介素-12通过核因子κB信号通路诱导T细胞上神经激肽-1受体的表达。
J Immunol. 2003 May 15;170(10):5003-7. doi: 10.4049/jimmunol.170.10.5003.
10
Regulation of the NK-1 receptor gene expression in human macrophage cells via an NF-kappa B site on its promoter.通过人巨噬细胞中NK-1受体基因启动子上的NF-κB位点对其基因表达进行调控。
Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2957-62. doi: 10.1073/pnas.0530112100. Epub 2003 Feb 19.

白细胞介素-12（IL-12）和IL-23诱导小鼠T细胞和巨噬细胞中P物质合成受IL-10和转化生长因子β调控。

Interleukin-12 (IL-12) and IL-23 induction of substance p synthesis in murine T cells and macrophages is subject to IL-10 and transforming growth factor beta regulation.

作者信息

Blum Arthur, Setiawan Tommy, Hang Long, Stoyanoff Korynn, Weinstock Joel V

机构信息

Division of Gastroenterology (233), Tufts New England Medical Center, Boston, MA 02111, USA.

出版信息

Infect Immun. 2008 Aug;76(8):3651-6. doi: 10.1128/IAI.00358-08. Epub 2008 May 27.

DOI:10.1128/IAI.00358-08
PMID:18505813
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2493212/
Abstract

Substance P is a tachykinin that enhances pathways of inflammation. Leukocytes at sites of intestinal inflammation make substance P. This study explored the role of interleukin-12 (IL-12), IL-23, and the regulatory cytokines IL-10 and transforming growth factor beta (TGF-beta) in controlling leukocyte substance P production. In murine schistosomiasis, it was found that IL-12 and IL-23 drive substance P gene expression and peptide synthesis in murine splenic T cells and macrophages, respectively. Cytokine induction of substance P synthesis both in T cells and in macrophages depends on intracellular NF-kappaB activation and is Stat4 independent. IL-10 inhibits T-cell substance P production, while TGF-beta blocks macrophage substance P expression. Intestinal macrophages also produce substance P, subject mostly to IL-23 and TGF-beta regulation. Hemokinin is another tachykinin with homology to substance P. Macrophages and T cells make hemokinin, but hemokinin production is not subject to IL-12 or IL-23 regulation.

摘要

P物质是一种速激肽，可增强炎症通路。肠道炎症部位的白细胞会产生P物质。本研究探讨了白细胞介素-12（IL-12）、IL-23以及调节性细胞因子IL-10和转化生长因子β（TGF-β）在控制白细胞P物质产生中的作用。在小鼠血吸虫病中，发现IL-12和IL-23分别驱动小鼠脾脏T细胞和巨噬细胞中P物质基因表达和肽合成。T细胞和巨噬细胞中P物质合成的细胞因子诱导均依赖于细胞内NF-κB激活，且不依赖于Stat4。IL-10抑制T细胞P物质产生，而TGF-β阻断巨噬细胞P物质表达。肠道巨噬细胞也产生P物质，主要受IL-23和TGF-β调节。血红蛋白是另一种与P物质具有同源性的速激肽。巨噬细胞和T细胞产生血红蛋白，但血红蛋白的产生不受IL-12或IL-23调节。