Mast cells contribute to initiation of autoantibody-mediated arthritis via IL-1

Nigrović, Peter A.; Binstadt, Bryce A; Monach, Paul A.; Johnsen, Alyssa; Gurish, Michael F.; Iwakura, Yoichiro; Benoist, Christophe; Mathis, Diane; Lee, David M.

doi:10.1073/pnas.0610852103

Cited by 167 publications

(197 citation statements)

References 55 publications

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“…1H) with K/BxN serum (in agreement with unpublished data discussed in Ref. 23). Similar results were reported for these two mouse strains in another passive model of arthritis (15).…”

Section: Resultssupporting

confidence: 76%

Cutting Edge: The Murine High-Affinity IgG Receptor FcγRIV Is Sufficient for Autoantibody-Induced Arthritis

Mancardi

Jönsson

Iannascoli

et al. 2011

The Journal of Immunology

107

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K/BxN serum-induced passive arthritis was reported to depend on the activation of mast cells, triggered by the activating IgG receptor FcγRIIIA, when engaged by IgG1 autoantibodies present in K/BxN serum. This view is challenged by the fact that FcγRIIIA-deficient mice still develop K/BxN arthritis and because FcγRIIIA is the only activating IgG receptor expressed by mast cells. We investigated the contribution of IgG receptors, IgG subclasses, and cells in K/BxN arthritis. We found that the activating IgG2 receptor FcγRIV, expressed only by monocytes/macrophages and neutrophils, was sufficient to induce disease. K/BxN arthritis occurred not only in mast cell-deficient Wsh mice, but also in mice whose mast cells express no activating IgG receptors. We propose that at least two autoantibody isotypes, IgG1 and IgG2, and two activating IgG receptors, FcγRIIIA and FcγRIV, contribute to K/BxN arthritis, which requires at least two cell types other than mast cells, monocytes/macrophages, and neutrophils.

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“…1H) with K/BxN serum (in agreement with unpublished data discussed in Ref. 23). Similar results were reported for these two mouse strains in another passive model of arthritis (15).…”

Section: Resultssupporting

confidence: 76%

Cutting Edge: The Murine High-Affinity IgG Receptor FcγRIV Is Sufficient for Autoantibody-Induced Arthritis

Mancardi

Jönsson

Iannascoli

et al. 2011

The Journal of Immunology

107

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“…Some of the positive immunomodulatory functions of mast cells that have been proposed based on in vitro studies have been confirmed in vivo using mast cell knock-in mice 1,54,[57][58][59][60][61][62][63][64][65][66][67][68][69][70] or in mice lacking specific mast-cell-associated proteases [26][27][28][32][33][34] or lacking specific protease enzymatic activity 11 (Table 1 ). In many of these studies, the end points assessed included the recruitment of particular immune cells, such as granulocytes 28,32,33,[57][58][59][60][61]63,64,[67][68][69][70] , DCs 62,64,65,71 or various subpopulations of lymphocytes 64,67,70,72 .…”

Section: Positive Immunomodulatory Functions In Vivomentioning

confidence: 93%

Immunomodulatory mast cells: negative, as well as positive, regulators of immunity

2008

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Section: Requirements For Disease In the Modelmentioning

confidence: 99%

“…They are required for the GPI-autoimmune model of arthritis (11). Mast celldeficient mouse strains (W/W v or Sl/Sl d ) are resistant to arthritis induction by serum transfer; mast cell transfer restores susceptibility in the W/W v strain (11). Proinflammatory cytokines, particularly interleukin-1␤ (IL-1␤), tumor necrosis factor ␣ (TNF␣), and IL-6 are up-regulated in arthritis (6,7).…”

Section: Requirements For Disease In the Modelmentioning

confidence: 99%

“…Proinflammatory cytokines, particularly interleukin-1␤ (IL-1␤), tumor necrosis factor ␣ (TNF␣), and IL-6 are up-regulated in arthritis (6,7). Whereas some TNF␣-deficient mouse strains can develop robust disease in the K/BxN mouse serum-transfer model, IL-1 Ϫ/Ϫ and IL-1 receptor (IL-1R) Ϫ/Ϫ mice are resistant (11). Intraperitoneal administration of IL-1␤, but not TNF␣, restores the arthritis susceptibility of W/W v mice.…”

Section: Requirements For Disease In the Modelmentioning

confidence: 99%

See 1 more Smart Citation

Systemic humoral autoimmunity but joint‐specific inflammation: The syndrome of rheumatoid arthritis

Wu¹,

Shih²,

Atkinson³

2007

Arthritis & Rheumatism

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Mast cells contribute to initiation of autoantibody-mediated arthritis via IL-1

Cited by 167 publications

References 55 publications

Cutting Edge: The Murine High-Affinity IgG Receptor FcγRIV Is Sufficient for Autoantibody-Induced Arthritis

Cutting Edge: The Murine High-Affinity IgG Receptor FcγRIV Is Sufficient for Autoantibody-Induced Arthritis

Immunomodulatory mast cells: negative, as well as positive, regulators of immunity

Systemic humoral autoimmunity but joint‐specific inflammation: The syndrome of rheumatoid arthritis

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