Mast cell numbers in rheumatoid synovial tissues

Malone, Daniel G.; Wilder, Ronald L.; Saavedra-Delgado, Ana Maria; Metcalfe, Dean D.

doi:10.1002/art.1780300202

Cited by 122 publications

(10 citation statements)

References 32 publications

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“…The synovium proliferates and grows in a manner similar to cancer tissue. MCs residing in synovial tissue are often in the activated, degranulated state (23, 25, 26). In allergic reactions, MCs are usually activated through their high‐affinity IgE receptors (FcɛRI).…”

Section: Mcs In Ramentioning

confidence: 99%

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Mast cells in the pathogenesis of rheumatic diseases and as potential targets for anti‐rheumatic therapy

Eklund

2007

Immunological Reviews

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Increasing evidence suggests that mast cells (MCs), in addition to acute allergic reactions, are involved in the pathogenesis of chronic inflammatory diseases and in particular in rheumatoid arthritis (RA). MCs reside in connective tissues and in synovial tissue of joints. They produce an array of proinflammatory mediators, tissue destructive proteases, and cytokines, most prominently tumor necrosis factor-alpha, which is one of the key cytokines in the pathogenesis of RA. MCs may also participate in the development of secondary or amyloid A amyloidosis, as the partial degradation of the serum amyloid A (SAA) protein by MCs leads to the generation of a highly amyloidogenic N-terminal fragment of SAA. MCs may contribute to the pathogenesis of connective tissue diseases, scleroderma, vasculitic syndromes, and systemic lupus erythematosus, although the data available are limited. Inhibition of the most important growth factor receptor of human MCs, c-Kit, by the selective tyrosine kinase inhibitor imatinib mesylate, induces apoptosis of synovial tissue MCs. As MCs are long-lived cells, induction of their apoptosis could be a feasible approach to inhibit their functions. Preliminary findings suggest that a drug that inhibits c-Kit could have anti-rheumatic activity in the treatment of patients with RA and spondyloarthropathies.

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Section: Mcs In Ramentioning

confidence: 99%

“…MCs often appear to be in an activated state in synovial tissue (23, 25, 26). In addition, increased levels of MC‐derived mediators, histamine and tryptase, have been detected in synovial fluids of RA patients, which also suggests that MCs in RA synovium are continuously activated (36, 37).…”

Section: Mcs In Ramentioning

confidence: 99%

Mast cells in the pathogenesis of rheumatic diseases and as potential targets for anti‐rheumatic therapy

Eklund

2007

Immunological Reviews

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“…Moreover, MCs are implicated to have a role in inflammatory diseases such as autoimmune arthritis 17 18 . Interestingly, both human patients with rheumatoid arthritis (RA) and mice subjected to the collagen-induced arthritis (CIA) RA model show increased numbers of MCs in the inflamed synovium 17 19 20 21 22 23 24 , suggesting that MCs contribute to this type of pathology. Indeed, there are several studies based on the use of MC-deficient animals that support a pathogenic role of MCs in various models of arthritis, both passively 25 and actively 18 induced.…”

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confidence: 99%

Activated mast cells promote differentiation of B cells into effector cells

Palm

Garcia-Faroldi

Lundberg

et al. 2016

Sci Rep

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Based on the known accumulation of mast cells (MCs) in B cell-dependent inflammatory diseases, including rheumatoid arthritis, we hypothesized that MCs directly modulate B cells. We show here that degranulated, and to a lesser extent naïve or IgE-sensitized, MCs activate both naïve and B cell receptor-activated B cells. This was shown by increased proliferation, blast formation, and expression of CD19, MHC class II and CD86 in the B cells. Further, MCs stimulated the secretion of IgM and IgG in IgM+ B cells, indicating that MCs can induce class-switch recombination in B cells. We also show that coculture of MCs with B cells promotes surface expression of L-selectin, a homing receptor, on the B cells. The effects of MCs on B cells were partly dependent on cell-cell contact and both follicular and marginal zone B cells could be activated by MCs. Our findings suggest that degranulated MCs support optimal activation of B cells, a finding that is in line with in vivo studies showing that MCs frequently degranulate in the context of B-cell driven pathologies such as arthritis. Together, our findings show that MCs have the capacity to differentiate B cells to effector cells.

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“…However, several observations that would be in favor of our concept exist: Malone et al [34] have reported on an inverse correlation between the number of MC and the amount of fibrin deposits in synovial tissue in patients with rheumatoid arthritis. In addition, the MC-dependent (rapid) fibrin deposition in experimental animals seems to resolve more rapidly as compared to an MC-independent fibrin deposition.…”

Section: Clinical Significancementioning

confidence: 88%

What Have Mast Cells To Do with Edema Formation, the Consecutive Repair and Fibrinolysis?

Valent¹,

Sillaber²,

Baghestanian³

et al. 1997

Int Arch Allergy Immunol

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Mast cells (MC) have been implicated in the activation of vascular endothelial cells, capillary leak formation, transmigration of white blood cells, and translocation of fibrinogen (and other plasma molecules) into the tissues, with consecutive edema formation. However, the mechanisms of repair that lead to tissue reconstitution after MC activation and edema formation have not been defined so far. In the present article, the possible contribution of MC to repair, in particular fibrinolysis, is discussed. Thus, accumulating evidence exists that human MC express and release the tissue-type plasminogen activator (tPA) in a constitutive manner. MC also express the urokinase receptor (uPAR) and heparin. Most importantly, however, MC lack plasminogen activator inhibitors (PAI-1, PAI-2, PAI-3). In line with this ‘pro-fibrinolytic’ profile of antigens, MC supernatants induce plasminogen-to-plasmin conversion and fibrin clot lysis in vitro. The c-kit ligand SCF upregulates uPAR expression, and the release of tPA from MC. These observations point to an important role of MC in endogenous fibrinolysis, a hitherto unrecognized (repair) function of this cell.

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Mast cell numbers in rheumatoid synovial tissues

Cited by 122 publications

References 32 publications

Mast cells in the pathogenesis of rheumatic diseases and as potential targets for anti‐rheumatic therapy

Mast cells in the pathogenesis of rheumatic diseases and as potential targets for anti‐rheumatic therapy

Activated mast cells promote differentiation of B cells into effector cells

What Have Mast Cells To Do with Edema Formation, the Consecutive Repair and Fibrinolysis?

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