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Infect Immun. 1998 Sep;66(9):4541-4. doi: 10.1128/IAI.66.9.4541-4544.1998.
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Nonopsonic binding of type III Group B Streptococci to human neutrophils induces interleukin-8 release mediated by the p38 mitogen-activated protein kinase pathway.B族链球菌III型对人中性粒细胞的非调理素性结合可诱导由p38丝裂原活化蛋白激酶途径介导的白细胞介素-8释放。
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本文引用的文献

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A coat of many complements.众多补体组成的一层膜。
Nat Med. 1997 Oct;3(10):1078-9. doi: 10.1038/nm1097-1078.
2
The 25-kDa soluble CD23 activates type III constitutive nitric oxide-synthase activity via CD11b and CD11c expressed by human monocytes.25千道尔顿可溶性CD23通过人单核细胞表达的CD11b和CD11c激活III型组成型一氧化氮合酶活性。
J Immunol. 1997 Jul 15;159(2):614-22.
3
Nonopsonic binding of Mycobacterium tuberculosis to human complement receptor type 3 expressed in Chinese hamster ovary cells.结核分枝杆菌与中国仓鼠卵巢细胞中表达的人补体受体3的非调理素结合。
Infect Immun. 1996 Dec;64(12):5373-83. doi: 10.1128/iai.64.12.5373-5383.1996.
4
Macrophage phagocytosis of virulent but not attenuated strains of Mycobacterium tuberculosis is mediated by mannose receptors in addition to complement receptors.除补体受体外,甘露糖受体介导巨噬细胞对结核分枝杆菌强毒株而非减毒株的吞噬作用。
J Immunol. 1993 Apr 1;150(7):2920-30.
5
Detection of Src homology 3-binding proteins, including paxillin, in normal and v-Src-transformed Balb/c 3T3 cells.在正常和v-Src转化的Balb/c 3T3细胞中检测包括桩蛋白在内的Src同源3结合蛋白。
J Biol Chem. 1993 Jul 15;268(20):14956-63.
6
Complement receptor-mediated uptake and tumor necrosis factor-alpha-mediated growth inhibition of Mycobacterium tuberculosis by human alveolar macrophages.人肺泡巨噬细胞通过补体受体介导的摄取及肿瘤坏死因子-α介导的结核分枝杆菌生长抑制作用
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Zymosan-triggered association of tyrosine phosphoproteins and lyn kinase with cytoskeleton in human monocytes.
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Zymosan-induced tyrosine phosphorylations in human monocytes. Role of protein kinase C.酵母聚糖诱导的人单核细胞酪氨酸磷酸化。蛋白激酶C的作用。
J Immunol. 1993 Jul 1;151(1):405-14.
9
Tyrosine phosphorylation is required for Fc receptor-mediated phagocytosis in mouse macrophages.酪氨酸磷酸化是小鼠巨噬细胞中Fc受体介导的吞噬作用所必需的。
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10
CD14 receptor-mediated uptake of nonopsonized Mycobacterium tuberculosis by human microglia.人小胶质细胞通过CD14受体介导对未被调理的结核分枝杆菌的摄取。
Infect Immun. 1995 Apr;63(4):1598-602. doi: 10.1128/iai.63.4.1598-1602.1995.

CR4在无血清情况下对结核分枝杆菌与人巨噬细胞结合及信号转导中的作用。

Role of CR4 in Mycobacterium tuberculosis-human macrophages binding and signal transduction in the absence of serum.

作者信息

Zaffran Y, Zhang L, Ellner J J

机构信息

Department of Medicine, Case Western Reserve University, and University Hospitals, Cleveland, Ohio 44106-4984, USA.

出版信息

Infect Immun. 1998 Sep;66(9):4541-4. doi: 10.1128/IAI.66.9.4541-4544.1998.

DOI:10.1128/IAI.66.9.4541-4544.1998
PMID:9712816
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108554/
Abstract

The beta2 integrin CR4 is involved in Mycobacterium tuberculosis phagocytosis by human mononuclear phagocytes through the opsonin C3bi. In this study, we demonstrate that M. tuberculosis can bind directly to monocyte-derived macrophages via CR4 in the absence of any opsonins. CR4-transfected CHO cells gave similar results, suggesting recognition by CR4 of bacterial structure. Furthermore, binding of M. tuberculosis transduced a potent signal, resulting in tyrosine phosphorylation of macrophage proteins, which was in part mediated by CR4.

摘要

β2整合素CR4通过调理素C3bi参与人单核吞噬细胞对结核分枝杆菌的吞噬作用。在本研究中,我们证明,在没有任何调理素的情况下,结核分枝杆菌可通过CR4直接与单核细胞衍生的巨噬细胞结合。转染CR4的CHO细胞也得到了类似结果,表明CR4可识别细菌结构。此外,结核分枝杆菌的结合传导了一个有效的信号,导致巨噬细胞蛋白的酪氨酸磷酸化,这部分是由CR4介导的。