RBL-2H3 cells are an imprecise model for mast cell mediator release

Passante, Egle; Ehrhardt, Carsten; Sheridan, Helen; Frankish, Neil

doi:10.1007/s00011-009-0028-4

Cited by 103 publications

(88 citation statements)

References 25 publications

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“…The interaction of allergens with IgE-sensitized mast cells stimulates cells to degranulate and release allergic mediators such as histamine, serotonin, β-hexosaminidase 37) and cytokines, including IL-4 and IL-5.…”

Section: Resultsmentioning

confidence: 99%

Mast Cell Stabilizing Effect of (−)-Elema-1,3,11(13)-trien-12-ol and Thujopsene from <i>Thujopsis dolabrata</i> Is Mediated by Down-Regulation of Interleukin-4 Secretion in Antigen-Induced RBL-2H3 Cells

Kim

Lee

et al. 2013

Biological & Pharmaceutical Bulletin

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Section: Resultsmentioning

confidence: 99%

Mast Cell Stabilizing Effect of (−)-Elema-1,3,11(13)-trien-12-ol and Thujopsene from <i>Thujopsis dolabrata</i> Is Mediated by Down-Regulation of Interleukin-4 Secretion in Antigen-Induced RBL-2H3 Cells

Kim

Lee

et al. 2013

Biological & Pharmaceutical Bulletin

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“…However, the experiments were performed using the RBL-2H3 cell line transfected with mutant C5aR2. This cell line lacks responsiveness to common GPCR ligands such as c48/80, C3a, and C5a (62). The possibility that C5aR2 can couple with PTx-insensitive Ga q proteins has not been explored.…”

Section: Discussionmentioning

confidence: 99%

The Novel Receptor C5aR2 Is Required for C5a-Mediated Human Mast Cell Adhesion, Migration, and Proinflammatory Mediator Production

Pundir

MacDonald

Kulka

2015

The Journal of Immunology

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C5a generated during complement activation possesses proinflammatory and immunoregulatory properties critical for the development and modulation of allergic immune responses. In immune cells, C5a mediates its effects through binding to two G protein–coupled receptors, C5aR1 and C5aR2. Mast cells are key effectors in allergic reactions, and decades of research have suggested that the majority of C5a effects on mast cells are mediated through C5aR1, whereas the expression and function of C5aR2 have not been explored. We demonstrated that the human mast cell line Laboratory of Allergic Diseases 2 (LAD2) expresses surface C5aR2 but not C5aR1, whereas CD34+ cell–derived primary mast cells do not express surface C5aR1 or C5aR2. Stem cell factor and IL-4 upregulated C5aR2 expression on LAD2 cells. Furthermore, C5a caused internalization of LAD2 cell-surface C5aR2. We therefore used LAD2 cells as a model to study C5a/C5aR2-induced biological responses and signaling in human mast cells. We found that whereas C5a was unable to induce degranulation, it stimulated GM-CSF, TNF, CXCL10, and CCL2 production. C5a caused ERK phosphorylation, a signaling molecule important in cytokine and chemokine generation. In addition, C5a stimulated adhesion and chemotaxis of mast cells. Wortmannin, an inhibitor of PI3K, and small interfering RNA against β-arrestin-2 blocked C5a-induced adhesion. Silencing of C5aR2 using lentiviral short hairpin RNA rendered the cells unresponsive to C5a-induced adhesion, chemotaxis, and mediator release, as well as ERK phosphorylation. Overall, this study reveals a novel role for C5aR2 in C5a-mediated activation of mast cells and demonstrates that C5aR2 ligation initiates a β-arrestin-2–, PI3K-, and ERK-dependent signaling pathway in these cells.

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“…RBL-2H3 cells treated with EPA solubilized in ethanol for 48 h showed increased degranulation and Syk phosphorylation on IgE/antigen stimulation [162]. RBL-2H3 cells are not a precise model of mast cells and Fc«RI signaling, because they have a different membrane molecule profile from primary mast cells and are considered to be closer to basophils [163,164]. In addition, Fc«RI expression in RBL-2H3 cells has not been consistent in different laboratories using the same culture protocol [163].…”

Section: N-3 Pufas and Fc«ri-mediated Mast Cell Activationmentioning

confidence: 99%

n-3 Polyunsaturated fatty acids and mast cell activation

Kulka

2015

Journal of Leukocyte Biology

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Mast cells are known to play a vital role in the development of inflammation in allergic responses. Recent studies have indicated that mast cell activation could be modulated by n-3 PUFAs, which have a wide range of well-documented health benefits. In our review, we summarize the recent findings and potential mechanisms of the effect of n-3 PUFAs on mast cell activation. This knowledge could provide new strategies for the development of therapeutic interventions for diseases mediated by mast cells.

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RBL-2H3 cells are an imprecise model for mast cell mediator release

Abstract: While RBL-2H3 cells may be useful as a model for mast cell IgE-mediated degranulation, other aspects may not be representative and they may share similarities with basophils rather than with other histamine-releasing cell types.

Cited by 103 publications

References 25 publications

Mast Cell Stabilizing Effect of (−)-Elema-1,3,11(13)-trien-12-ol and Thujopsene from <i>Thujopsis dolabrata</i> Is Mediated by Down-Regulation of Interleukin-4 Secretion in Antigen-Induced RBL-2H3 Cells

Mast Cell Stabilizing Effect of (−)-Elema-1,3,11(13)-trien-12-ol and Thujopsene from <i>Thujopsis dolabrata</i> Is Mediated by Down-Regulation of Interleukin-4 Secretion in Antigen-Induced RBL-2H3 Cells

The Novel Receptor C5aR2 Is Required for C5a-Mediated Human Mast Cell Adhesion, Migration, and Proinflammatory Mediator Production

n-3 Polyunsaturated fatty acids and mast cell activation

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