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Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages. / Vogelpoel, Lisa T. C.; Hansen, Ivo S.; Rispens, Theo et al.

In: Nature communications, Vol. 5, 2014, p. 5444.

Research output: Contribution to journal › Article › Academic › peer-review

Harvard

Vogelpoel, LTC, Hansen, IS, Rispens, T, Muller, FJM, van Capel, TMM, Turina, MC, Vos, JB, Baeten, DLP, Kapsenberg, ML, de Jong, EC & den Dunnen, J 2014, 'Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages', Nature communications, vol. 5, pp. 5444. https://doi.org/10.1038/ncomms6444

APA

Vogelpoel, L. T. C., Hansen, I. S., Rispens, T., Muller, F. J. M., van Capel, T. M. M., Turina, M. C., Vos, J. B., Baeten, D. L. P., Kapsenberg, M. L., de Jong, E. C., & den Dunnen, J. (2014). Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages. Nature communications, 5, 5444. https://doi.org/10.1038/ncomms6444

Vancouver

Vogelpoel LTC, Hansen IS, Rispens T, Muller FJM, van Capel TMM, Turina MC et al. Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages. Nature communications. 2014;5:5444. doi: 10.1038/ncomms6444

Author

Vogelpoel, Lisa T. C. ; Hansen, Ivo S. ; Rispens, Theo et al. / Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages. In: Nature communications. 2014 ; Vol. 5. pp. 5444.

BibTeX

@article{5da7827d88b34327b1c1ecce48f7d16a,
title = "Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages",
abstract = "M2 macrophages suppress inflammation in numerous disorders, including tumour formation, infection and obesity. However, the exact role of M2 macrophages in the context of several other diseases is still largely undefined. We here show that human M2 macrophages promote inflammation instead of suppressing inflammation on simultaneous exposure to complexed IgG (c-IgG) and TLR ligands, as occurs in the context of diseases such as rheumatoid arthritis (RA). c-IgG-TLR ligand co-stimulation of M2 macrophages selectively amplifies production of pro-inflammatory cytokines TNF-α, IL-1β and IL-6 and promotes Th17 responses, which all play a critical role in RA pathology. Induction of pro-inflammatory cytokines on c-IgG co-stimulation mainly depends on Fc gamma receptor IIa (FcγRIIa), which selectively amplifies cytokine gene transcription and induces caspase-1 activation. These data indicate that FcγR-TLR cross-talk may be targeted for treatment to attenuate inflammation in RA, by restoring the anti-inflammatory function of M2 macrophages",
author = "Vogelpoel, {Lisa T. C.} and Hansen, {Ivo S.} and Theo Rispens and Muller, {Femke J. M.} and {van Capel}, {Toni M. M.} and Turina, {Maureen C.} and Vos, {Joost B.} and Baeten, {Dominique L. P.} and Kapsenberg, {Martien L.} and {de Jong}, {Esther C.} and {den Dunnen}, Jeroen",
year = "2014",
doi = "10.1038/ncomms6444",
language = "English",
volume = "5",
pages = "5444",
journal = "Nature communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - Fc gamma receptor-TLR cross-talk elicits pro-inflammatory cytokine production by human M2 macrophages

AU - Vogelpoel, Lisa T. C.

AU - Hansen, Ivo S.

AU - Rispens, Theo

AU - Muller, Femke J. M.

AU - van Capel, Toni M. M.

AU - Turina, Maureen C.

AU - Vos, Joost B.

AU - Baeten, Dominique L. P.

AU - Kapsenberg, Martien L.

AU - de Jong, Esther C.

AU - den Dunnen, Jeroen

PY - 2014

Y1 - 2014

N2 - M2 macrophages suppress inflammation in numerous disorders, including tumour formation, infection and obesity. However, the exact role of M2 macrophages in the context of several other diseases is still largely undefined. We here show that human M2 macrophages promote inflammation instead of suppressing inflammation on simultaneous exposure to complexed IgG (c-IgG) and TLR ligands, as occurs in the context of diseases such as rheumatoid arthritis (RA). c-IgG-TLR ligand co-stimulation of M2 macrophages selectively amplifies production of pro-inflammatory cytokines TNF-α, IL-1β and IL-6 and promotes Th17 responses, which all play a critical role in RA pathology. Induction of pro-inflammatory cytokines on c-IgG co-stimulation mainly depends on Fc gamma receptor IIa (FcγRIIa), which selectively amplifies cytokine gene transcription and induces caspase-1 activation. These data indicate that FcγR-TLR cross-talk may be targeted for treatment to attenuate inflammation in RA, by restoring the anti-inflammatory function of M2 macrophages

AB - M2 macrophages suppress inflammation in numerous disorders, including tumour formation, infection and obesity. However, the exact role of M2 macrophages in the context of several other diseases is still largely undefined. We here show that human M2 macrophages promote inflammation instead of suppressing inflammation on simultaneous exposure to complexed IgG (c-IgG) and TLR ligands, as occurs in the context of diseases such as rheumatoid arthritis (RA). c-IgG-TLR ligand co-stimulation of M2 macrophages selectively amplifies production of pro-inflammatory cytokines TNF-α, IL-1β and IL-6 and promotes Th17 responses, which all play a critical role in RA pathology. Induction of pro-inflammatory cytokines on c-IgG co-stimulation mainly depends on Fc gamma receptor IIa (FcγRIIa), which selectively amplifies cytokine gene transcription and induces caspase-1 activation. These data indicate that FcγR-TLR cross-talk may be targeted for treatment to attenuate inflammation in RA, by restoring the anti-inflammatory function of M2 macrophages

U2 - 10.1038/ncomms6444

DO - 10.1038/ncomms6444

M3 - Article

C2 - 25392121

VL - 5

SP - 5444

JO - Nature communications

JF - Nature communications

SN - 2041-1723

ER -

ID: 2501199