Regulation of Fcgamma receptors and immunoglobulin G-mediated phagocytosis in mouse microglia.
Regulation of Fcgamma receptors and immunoglobulin G-mediated phagocytosis in mouse microglia.
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DOI：
10.1016/j.neulet.2009.08.013
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发表时间：
2009-10-16
影响因子：
2.5
通讯作者：
Weinstein JR
中科院分区：
文献类型：
--
作者：
Quan Y;Möller T;Weinstein JR
As resident macrophages in the CNS, microglia can transform from a surveillance state to an activated phenotype in response to brain injury. During this transition microglia become highly capable phagocytic cells. Invading pathogens undergo opsonization with immunoglobulins and microglia recognize these opsonized pathogens through interaction with their cognate Fc receptors. In mice, both FcγRI and FcγRIIb receptors are involved in IgG-mediated phagocytosis of opsonzied pathogens. At sites of inflammation, microglial activity is regulated by T-cell derived cytokines. Here we first investigated the effects of IFN-γ, IL-4, IL-13 and GM-CSF on expression of FcγRI and FcγRIIb mRNA levels in both primary microglia and microglial cell line N9. Using quantitative real-time PCR we show that IFN-γ induced a four-fold increase in the mRNA level of FcγRI but did not induce changes in FcγRIIb expression. IL-4 and IL-13 induced approximately two-fold increases in expression of FcγRIIb mRNA, but had no effect on FcγRI expression. GM-CSF increased both FcγRI and FcγRIIb mRNA expression. We then characterized the ability of these same cytokines to regulate phagocytosis of immune complexes composed of IgG and the bacteria Staphylococcus aureus. IFN-γ and GM-CSF both induced approximately two-fold increases in IgG-mediated phagocytosis whereas IL-4 and IL-13 both decreased IgG-mediated phagocytosis by about one-third. None of the cytokines influenced basal levels of phagocytosis. These findings demonstrate a highly selective cytokine-induced regulation of both phagocytosis-related Fcγ receptor subtypes and IgG-mediated phagocytosis itself in microglia. This selective regulation has implications for our understanding of the pathophysiology of CNS infection and autoimmune disease.
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影响因子：
5.3
作者：
Ponomarev, Eugene D.;Maresz, Katarzyna;Dittel, Bonnie N.
通讯作者：
Dittel, Bonnie N.
影响因子：
15.9
作者：
Boruchov, AM;Heller, G;Young, JW
通讯作者：
Young, JW
影响因子：
32.4
作者：
Barnes, N;Gavin, AL;Hogarth, PM
通讯作者：
Hogarth, PM
DOI：
10.1084/jem.189.1.179
发表时间：
1999-01-04
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Clynes R;Maizes JS;Guinamard R;Ono M;Takai T;Ravetch JV
通讯作者：
Ravetch JV
影响因子：
6
作者：
Maña, P;Liñares, D;Willenborg, D
通讯作者：
Willenborg, D