Literature DB >> 19732955

Innate immune responses of primary murine macrophage-lineage cells and RAW 264.7 cells to ligands of Toll-like receptors 2, 3, and 4.

Londa J Berghaus1, James N Moore, David J Hurley, Michel L Vandenplas, Barbara P Fortes, Margreet A Wolfert, Geert-Jan Boons.   

Abstract

Although studies have been performed to characterize responses of macrophages from individual anatomical sites (e.g., alveolar macrophages) or of murine-derived macrophage cell lines to microbial ligands, few studies compare these cell types in terms of phenotype and function. We directly compared the expression of cell surface markers and functional responses of primary cultures of three commonly used cells of monocyte-macrophage lineage (splenic macrophages, bone marrow-derived macrophages, and bone marrow-derived dendritic cells) with those of the murine-leukemic monocyte-macrophage cell line, RAW 264.7. We hypothesized that RAW 264.7 cells and primary bone marrow-derived macrophages would be similar in phenotype and would respond similarly to microbial ligands that bind to either Toll-like receptors 2, 3, and 4. Results indicate that RAW 264.7 cells most closely mimic bone marrow-derived macrophages in terms of cell surface receptors and response to microbial ligands that initiate cellular activation via Toll-like receptors 3 and 4. However, caution must be applied when extrapolating findings obtained with RAW 264.7 cells to those of other primary macrophage-lineage cells, primarily because phenotype and function of the former cells may change with continuous culture. Copyright 2009 Elsevier Ltd. All rights reserved.

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Year:  2009        PMID: 19732955      PMCID: PMC2888975          DOI: 10.1016/j.cimid.2009.07.001

Source DB:  PubMed          Journal:  Comp Immunol Microbiol Infect Dis        ISSN: 0147-9571            Impact factor:   2.268


  23 in total

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Review 2.  Role of Toll-like receptors in inflammatory response in macrophages.

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Review 3.  Toll-like receptor signalling.

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4.  Differential roles of Toll-like receptors in the elicitation of proinflammatory responses by macrophages.

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