
NCBI . NLM . NIH . GOV {
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Title[redir]:
Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance - PMC
Description:
As an essential component of innate immunity, macrophages have multiple functions in both inhibiting or promoting cell proliferation and tissue repair. Diversity and plasticity are hallmarks of macrophages. Classical M1 and alternative M2 activation ...
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Keywords {🔍}
macrophages, doi, pubmed, google, scholar, macrophage, polarization, activation, pmc, article, free, signaling, immunol, phenotype, expression, tlr, receptor, inflammatory, cells, role, socs, factor, genes, nfκb, nod, cell, response, inflammation, proinflammatory, stat, responses, pathway, human, biol, immune, cytokine, transcription, hifα, tissue, found, mirnas, gene, mice, nat, jimmunol, functional, involved, tumor, including, irf,
Topics {✒️}
granulocyte-macrophage colony-stimulating factor γ-d-glutamyl-meso-diaminopimelic acid low-density lipoprotein receptor-knockout nf-κb-dependent pro-inflammatory genes nf-κb/hif-1α-dependent transcription common beta chain il-4rα/stat6-dependent m2 differentiation nf-κb p65/p50 heterodimer long-lasting anti-tumor immunity gm-csf-treated monocytes showed cytosolic nucleotide-binding receptors nf-κb/i-κb complex receptor-induced cytokine-receptor cascades promote tnfalpha-dependent growth pro-angiogenic m2-polarized phenotype pro-inflammatory cytokines [ifn-γ pmc beta search tumor necrosis factor-α endotoxin-induced differential cross-regulation gm-csf include regulating myeloid cell-specific deletion nod-induced nf-kappab activation ifn-β-dependent signaling pathways p50 nf-κb homodimer tumor-derived lactic acid hif-2α oligomerization domain tumour-derived lactic acid nf-kappab-dependent induction gm-csf deficient mice gm-csf receptor forms signal-regulatory protein α retinoic acid-induce gene m2-type responses describe m2-polarizing irf-4 axis process include c-myc rsv-induced lung injury pro-inflammatory m1 phenotype high-resolution transcriptome profile impaired nf-κb activation receptor-mediated immune responses macrophage m1–m2 polarization macrophage pro-inflammatory response extracellular signal-regulated kinase irf/stat signaling pathways myeloid cell-mediated inflammation pathogen-induced process detected precursors pro-il-1β c-type lectin signaling canonical irf/stat signaling tnf-induced macrophage polarization
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