A Pathogenetic Role for Mast Cells in Experimental Crescentic Glomerulonephritis

Timoshanko, Jennifer R.; Kitching, A. Richard; Semple, Timothy; Tipping, Peter G.; Holdsworth, Stephen R.

doi:10.1681/asn.2005080799

Cited by 57 publications

(40 citation statements)

References 45 publications

(35 reference statements)

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“…Increasing evidence suggests that MCs play critical roles in IgGdependent tissue-specific autoimmune diseases, including murine models of multiple sclerosis, RA, bullous pemphigoid, and glomerulonephritis (41)(42)(43)(44). In RA, circulating IgG isotype autoantibodies and immune complexes can activate synovial MCs through FcγRs (19), triggering release of inflammatory cytokines including TNF, IL-1β, and IL-17.…”

Section: Discussionmentioning

confidence: 99%

JNK1 controls mast cell degranulation and IL-1β production in inflammatory arthritis

Gumá

Kashiwakura

Crain

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Rheumatoid arthritis (RA) is a chronic inflammatory disease marked by bone and cartilage destruction. Current biologic therapies are beneficial in only a portion of patients; hence small molecules targeting key pathogenic signaling cascades represent alternative therapeutic strategies. Here we show that c-Jun N-terminal kinase (JNK) 1, but not JNK2, is critical for joint swelling and destruction in a serum transfer model of arthritis. The proinflammatory function of JNK1 requires bone marrow-derived cells, particularly mast cells. Without JNK1, mast cells fail to degranulate efficiently and release less IL-1β after stimulation via Fcγ receptors (FcγRs). Pharmacologic JNK inhibition effectively prevents arthritis onset and abrogates joint swelling in established disease. Hence, JNK1 controls mast cell degranulation and FcγR-triggered IL-1β production, in addition to regulating cytokine and matrix metalloproteinase biosynthesis, and is an attractive therapeutic target in inflammatory arthritis.

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Section: Discussionmentioning

confidence: 99%

JNK1 controls mast cell degranulation and IL-1β production in inflammatory arthritis

Gumá

Kashiwakura

Crain

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…Most studies have suggested that a reduction of mast cells, or their typical enzyme chymase, increases fibrosis (52)(53)(54)(55)(56), whereas others suggest the opposite (57,58). Thus, the potential therapeutic value of mast cell manipulation in fibrosis is uncertain (23,59).…”

Section: The Role Of Immune Cellsmentioning

confidence: 99%

Renal Allograft Fibrosis: Biology and Therapeutic Targets

Floege

2015

American Journal of Transplantation

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“…Timoshanko et al 122 demonstrated a role for mast cells in inducing functional renal injury by the mechanism of infiltrating mast cells that recruit DTH effector leukocytes. These local effects were comparable to studies showing a role for mast cells in dermal DTH.…”

Section: Role Of Mast Cells In Inflammatory and Autoimmune Kidney Dismentioning

confidence: 99%

Role of Mast Cells in Progressive Renal Diseases

Holdsworth¹,

Summers²

2008

Journal of the American Society of Nephrology

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116

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A Pathogenetic Role for Mast Cells in Experimental Crescentic Glomerulonephritis

Abstract: Mast cells infiltrate kidneys of humans with crescentic glomerulonephritis (GN),

Cited by 57 publications

References 45 publications

JNK1 controls mast cell degranulation and IL-1β production in inflammatory arthritis

JNK1 controls mast cell degranulation and IL-1β production in inflammatory arthritis

Renal Allograft Fibrosis: Biology and Therapeutic Targets

Role of Mast Cells in Progressive Renal Diseases

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