ArticleNeurobiology of disease2007
Interleukin 10 and TNFalpha synergistically enhance the expression of the G protein-coupled formylpeptide receptor 2 in microglia.
Article in Neurobiology of disease, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.International immunopharmacology · 2023Review
- Human endogenous retrovirus W family envelope protein (HERV-W env) facilitates the production of TNF-α and IL-10 by inhibiting MyD88s in glial cells.Archives of virology · 2021Article
- Importance of GPCR-Mediated Microglial Activation in Alzheimer's Disease.Frontiers in cellular neuroscience · 2018Review
- Microglial Aβ receptors in Alzheimer's disease.Cellular and molecular neurobiology · 2015Review
- Nonredundant protective properties of FPR2/ALX in polymicrobial murine sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Toll-like receptors are key players in neurodegeneration.International immunopharmacology · 2011Review
- Interleukin 4 induces the apoptosis of mouse microglial cells by a caspase-dependent mechanism.Neurobiology of disease · 2011Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Microglia are important participants in inflammatory responses in the central nervous system. We previously observed that tumor necrosis factor alpha (TNFalpha) induces the expression of the formylpeptide receptor mFPR2 on microglial cells. This chemoattractant receptor mediates microglial cell chemotaxis in response to a variety of peptides, including amyloid beta peptide (Abeta(42)), a major pathogenic factor in Alzheimer's disease (AD). In search for agents that regulate microglial activation, we unexpectedly found that IL-10 enhanced the expression of mFPR2 on TNFalpha-activated microglia. This was associated with a markedly increased microglial chemotaxis to Abeta(42) and its endocytosis via mFPR2. Mechanistic studies revealed that the synergistic effect of IL-10 on TNFalpha-induction of mFPR2 in microglia was dependent on activation of p38 MAPK. Our results suggest that IL-10 may affect the pathogenic process of AD by up-regulating mFPR2 and thus favoring the recognition and internalization of Abeta(42) by activated microglial cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.