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巨噬细胞受体的相互作用与调节

Interaction and regulation of macrophage receptors.

作者信息

Ezekowitz R A, Gordon S

出版信息

Ciba Found Symp. 1986;118:127-36. doi: 10.1002/9780470720998.ch9.

DOI:10.1002/9780470720998.ch9
PMID:3089710
Abstract

Macrophages express distinct plasma membrane receptors for different isotypes of immunoglobulin, bear at least two receptors for cleaved third complement component (CR1 and CR3) and have a lectin-like receptor that mediates endocytosis of glycoproteins or glycoconjugates with terminal mannose or fucose residues (MFR). Interferon-gamma, a macrophage-activating factor, induces effects common to other interferons as well as having unique effects on cell function. The down-regulation of MFR, induction of IgG2a Fc receptors and Class II antigens and enhanced production of superoxide and hydrogen peroxide can be considered interferon-gamma-specific effects on macrophages. Previous reports described synergism of various interferon preparations in anticellular and antiviral effects. However, interferon-alpha/beta can selectively antagonize the down-regulation of macrophage MFR by interferon-gamma. The macrophage MFR and CR3 also play a synergistic role in the uptake of zymosan and Leishmania donovani in the absence of serum. The receptors may act independently or in concert. Cleaved third complement components can be specifically eluted from zymosan particles in the absence of exogenous complement and are derived from the macrophages themselves. These studies indicate a role for macrophage complement in local opsonization of pathogens at extravascular sites and focus on the role of the tissue macrophage in first-line host defence.

摘要

巨噬细胞表达针对不同免疫球蛋白同种型的独特质膜受体,带有至少两种针对裂解的第三补体成分的受体(CR1和CR3),并具有一种凝集素样受体,该受体介导对带有末端甘露糖或岩藻糖残基的糖蛋白或糖缀合物的内吞作用(MFR)。γ干扰素是一种巨噬细胞激活因子,它既能诱导与其他干扰素共有的效应,也能对细胞功能产生独特的影响。MFR的下调、IgG2a Fc受体和II类抗原的诱导以及超氧化物和过氧化氢产生的增强,可被视为γ干扰素对巨噬细胞的特异性作用。先前的报道描述了各种干扰素制剂在抗细胞和抗病毒作用中的协同作用。然而,α/β干扰素可以选择性地拮抗γ干扰素对巨噬细胞MFR的下调作用。在无血清的情况下,巨噬细胞MFR和CR3在酵母聚糖和杜氏利什曼原虫的摄取中也发挥协同作用。这些受体可能独立起作用或协同发挥作用。在没有外源性补体的情况下,裂解的第三补体成分可以从酵母聚糖颗粒中特异性洗脱出来,并且它们来源于巨噬细胞自身。这些研究表明巨噬细胞补体在血管外部位病原体的局部调理作用中发挥作用,并聚焦于组织巨噬细胞在一线宿主防御中的作用。

相似文献

1
Interaction and regulation of macrophage receptors.巨噬细胞受体的相互作用与调节
Ciba Found Symp. 1986;118:127-36. doi: 10.1002/9780470720998.ch9.
2
Macrophage complement and lectin-like receptors bind Leishmania in the absence of serum.在无血清情况下,巨噬细胞补体和凝集素样受体可结合利什曼原虫。
J Exp Med. 1985 Jul 1;162(1):324-31. doi: 10.1084/jem.162.1.324.
3
Role of macrophage complement and lectin-like receptors in binding Leishmania parasites to host macrophages.巨噬细胞补体和凝集素样受体在利什曼原虫与宿主巨噬细胞结合中的作用。
Immunol Lett. 1985;11(3-4):227-32. doi: 10.1016/0165-2478(85)90172-5.
4
Local opsonization by secreted macrophage complement components. Role of receptors for complement in uptake of zymosan.分泌型巨噬细胞补体成分介导的局部调理作用。补体受体在酵母聚糖摄取中的作用。
J Exp Med. 1984 Jan 1;159(1):244-60. doi: 10.1084/jem.159.1.244.
5
Interaction of human monocytes, macrophages, and polymorphonuclear leukocytes with zymosan in vitro. Role of type 3 complement receptors and macrophage-derived complement.人单核细胞、巨噬细胞和多形核白细胞与酵母聚糖的体外相互作用。3型补体受体和巨噬细胞衍生补体的作用。
J Clin Invest. 1985 Dec;76(6):2368-76. doi: 10.1172/JCI112249.
6
Interferon alpha/beta selectively antagonises down-regulation of mannosyl-fucosyl receptors on activated macrophages by interferon gamma.
Biochem Biophys Res Commun. 1986 Apr 29;136(2):737-44. doi: 10.1016/0006-291x(86)90501-2.
7
Receptors and recognition mechanisms of Leishmania species.利什曼原虫属的受体与识别机制
Trans R Soc Trop Med Hyg. 1985;79(5):606-12. doi: 10.1016/0035-9203(85)90166-x.
8
Roles of CR3 and mannose receptors in the attachment and ingestion of Leishmania donovani by human mononuclear phagocytes.CR3和甘露糖受体在人单核吞噬细胞对杜氏利什曼原虫的黏附和摄取中的作用。
Infect Immun. 1988 Feb;56(2):363-9. doi: 10.1128/iai.56.2.363-369.1988.
9
Evidence that Leishmania donovani utilizes a mannose receptor on human mononuclear phagocytes to establish intracellular parasitism.杜氏利什曼原虫利用人类单核吞噬细胞上的甘露糖受体来建立细胞内寄生关系的证据。
J Immunol. 1986 Jun 15;136(12):4681-8.
10
Phagocytosis of Mycobacterium leprae by human monocyte-derived macrophages is mediated by complement receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18) and IFN-gamma activation inhibits complement receptor function and phagocytosis of this bacterium.人单核细胞衍生巨噬细胞对麻风分枝杆菌的吞噬作用由补体受体CR1(CD35)、CR3(CD11b/CD18)和CR4(CD11c/CD18)介导,而γ干扰素激活会抑制补体受体功能及该细菌的吞噬作用。
J Immunol. 1991 Sep 15;147(6):1983-94.

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