ArticleInflammation2004
Signaling pathways for Fc gamma receptor-stimulated tumor necrosis factor-alpha secretion and respiratory burst in RAW 264.7 macrophages.
Article in Inflammation, 2004. 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Impact of surface receptors TLR2, CR3, and FcγRIII onInfection and immunity · 2024Article
- FcγR-driven release of IL-6 by macrophages requires NOX2-dependent production of reactive oxygen species.The Journal of biological chemistry · 2013Article
- Article
- Protein kinase C and toll-like receptor signaling.Enzyme research · 2011Article
- Brucella melitensis, B. neotomae and B. ovis elicit common and distinctive macrophage defense transcriptional responses.Experimental biology and medicine (Maywood, N.J.) · 2009Article
- Targeting of protein kinase C-epsilon during Fcgamma receptor-dependent phagocytosis requires the epsilonC1B domain and phospholipase C-gamma1.Molecular biology of the cell · 2006Article
- Protein kinase C-alpha mediates TNF release process in RBL-2H3 mast cells.British journal of pharmacology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fc gamma receptor (Fc gammaR) signaling mediates several important macrophage functions including cytokine secretion and respiratory burst. The present study describes the development of a model using the macrophage cell line, RAW 264.7 for studying Fc gammaR-stimulated tumor necrosis factor-alpha (TNF-alpha) secretion and hydrogen peroxide (H2O2) production. In unprimed cells these functions were low but pretreatment with interferon-gamma augmented Fc gammaR-stimulated TNF-alpha secretion and H2O2 production to levels that were about half that caused by lipopolysaccharide (LPS) and zymosan, respectively. Studies on the signaling pathways found that TNF-alpha secretion stimulated by either Fc gammaR or LPS was decreased by inhibitors of PKC, MAPK p42/p44, and MAPK p38. TNF-alpha secretion was also reduced by the combination of PLC and PLD inhibitors but not by the individual inhibitors alone. H2O2 production stimulated by either Fc gammaR or zymosan was blocked by inhibitors of PKC, PLC, PLD, and MAPK p42/44 but not by MAPK p38. Thus, interferon-gamma treated RAW 264.7 cells are a model of inflammatory macrophages and are well suited for further study of these signaling pathways.
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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.