Mast cells as sentinels of innate immunity

Galli, Stephen J.; Maurer, Marcus; Lantz, Chris S.

doi:10.1016/s0952-7915(99)80010-7

Cited by 358 publications

(261 citation statements)

References 62 publications

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“…6). This demonstration of a functional high-affinity IgG receptor on mast cells may help explain in vivo observations which document the participation of the mast cells in host defense mechanisms against bacteria (9) and suggests that aggregation of the high-affinity receptors for IgG should be considered as a possible mechanism by which mast cells could be recruited to contribute to inflammation associated with viral diseases which induce IFN-␥ production (27).…”

Section: Discussionmentioning

confidence: 85%

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

Okayama

Kirshenbaum

Metcalfe

2000

The Journal of Immunology

170

152

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Biologically relevant activation of human mast cells through Fc receptors is believed to occur primarily through the high-affinity IgE receptor FcεRI. However, the demonstration in animal models that allergic reactions do not necessarily require Ag-specific IgE, nor the presence of a functional IgE receptor, and the clinical occurrence of some allergic reactions in situations where Ag-specific IgE appears to be lacking, led us to examine the hypothesis that human mast cells might express the high-affinity IgG receptor FcγRI and in turn be activated through aggregation of this receptor. We thus first determined by RT-PCR that resting human mast cells exhibit minimal message for FcγRI. We next found that IFN-γ up-regulated the expression of FcγRI. This was confirmed by flow cytometry, where FcγRI expression on human mast cells was increased from ∼2 to 44% by IFN-γ exposure. FcεRI, FcγRII, and FcγRIII expression was not affected. Scatchard plots were consisted with these data where the average binding sites for monomeric IgG1 (Ka = 4–5 × 108 M−1) increased from ∼2,400 to 12,100–17,300 per cell. Aggregation of FcγRI on human mast cells, and only after IFN-γ exposure, led to significant degranulation as evidenced by histamine release (24.5 ± 4.4%): and up-regulation of mRNA expression for specific cytokines including TNF-α, GM-CSF, IL-3 and IL-13. These findings thus suggest another mechanism by which human mast cells may be recruited into the inflammatory processes associated with some immunologic and infectious diseases.

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Section: Discussionmentioning

confidence: 85%

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

Okayama

Kirshenbaum

Metcalfe

2000

The Journal of Immunology

170

152

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“…It is now clear that this view was too limited as we have begun to appreciate the function of mast cells in innate immunity and a possible role in autoimmune disease [8,9]. Mast cels are multifunctional, tissue-dwelling cells [20] and a potential source of proinflammatory cytokines and chemotactic mediators [21] which are decisive in initiating the immune and inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

“…However, tissue-resident mast cells are exposed in the inflammatory sites to the products of a variety of infectious agents either by opsonin-dependent mechanisms or via direct binding to parasites or bacteria [7,8]. In addition, autoantibodies and complement factors bind to mast cells which prompt them to dump their cytokines and other inflammatory chemicals, thereby calling in the inflammatory cells [7,9].…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress stimulates IL‐4 and IL‐6 production in mast cells by an APE/Ref‐1‐dependent pathway

Frossi

Carli

Daniël³

et al. 2003

Eur J Immunol

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“…Despite the well-characterized role of FcεRI in mast cell activation [14], a variety of other agonists can activate mast cells. These include complement factors (e.g., C5a), lipid mediators (e.g., prostaglandins, leukotrienes), neuropeptides (e.g., substance P (SP), neurotensin), hormones (e.g., somatostatin), cytokines, chemokines, microbial products (e.g., lipopolysaccharide (LPS) or peptidoglycan), as well as extracellular nucleotides [15][16][17].…”

Section: Mast Cellsmentioning

confidence: 99%

“…Th2 cells, in turn, secrete a number of mediators and provide additional co-stimulatory signals that induce B cells to the production of allergen-specific IgE [90]. ND not detected Mast cells play an important role in the pathophysiology of asthma as effector cells through their chronic activation by IgE and allergens [13,15,16]. To fulfill this role, mast cells not only secrete a plethora of bronchospastic and proinflammatory mediators, shift Th1/Th2 balance toward the differentiation and expansion of Th2 cells, modulate antigen presentation by dendritic cells, and govern proliferation and activation of eosinophils [13,88,90] but also infiltrate the airway smooth muscle layer where they contribute to the increased ATP concentration in airways (Fig.…”

Section: Purinergic Signaling In Allergic Airway Inflammation: Focus mentioning

confidence: 99%

P2 receptor-mediated signaling in mast cell biology

Bulanova

Bulfone–Paus∥

2009

Purinergic Signalling

100

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Mast cells are widely recognized as effector cells of allergic inflammatory reactions. They contribute to the pathogenesis of different chronic inflammatory diseases, wound healing, fibrosis, thrombosis/fibrinolysis, and antitumor immune responses. In this paper, we summarized the role of P2X and P2Y receptors in mast cell activation and effector functions. Mast cells are an abundant source of ATP which is stored in their granules and secreted upon activation. We discuss the contribution of mast cells to the extracellular ATP release and to the maintenance of extracellular nucleotides pool. Recent publications highlight the importance of purinergic signaling for the pathogenesis of chronic airway inflammation. Therefore, the role of ATP and P2 receptors in allergic inflammation with focus on mast cells was analyzed. Finally, ATP functions as mast cell autocrine/paracrine factor and as messenger in intercellular communication between mast cells, nerves, and glia in the central nervous system.

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Mast cells as sentinels of innate immunity

Cited by 358 publications

References 62 publications

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

Oxidative stress stimulates IL‐4 and IL‐6 production in mast cells by an APE/Ref‐1‐dependent pathway

P2 receptor-mediated signaling in mast cell biology

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