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The ingenious mast cell: Contemporary insights into mast cell behavior and function

Dahlin, Joakim S., Maurer, Marcus, Metcalfe, Dean D., Pejler, Gunnar, Sagi‐Eisenberg, Ronit, Nilsson, Gunnar·2022·Allergy
DOI 10.1111/all.14881
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Abstract

Mast cells are (in)famous for their role in allergic diseases, but the physiological and pathophysiological roles of this ingenious cell are still not fully understood. Mast cells are important for homeostasis and surveillance of the human system, recognizing both endogenous and exogenous agents, which induce release of a variety of mediators acting on both immune and non‐immune cells, including nerve cells, fibroblasts, endothelial cells, smooth muscle cells, and epithelial cells. During recent years, clinical and experimental studies on human mast cells, as well as experiments using animal models, have resulted in many discoveries that help decipher the function of mast cells in health and disease. In this review, we focus particularly on new insights into mast cell biology, with a focus on mast cell development, recruitment, heterogeneity, and reactivity. We also highlight the development in our understanding of mast cell‐driven diseases and discuss the development of novel strategies to treat such conditions.

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Image 1
CC-BY-NC-ND · From the PDF
FIGURE 1 Mast cell activation pathways and release of mediators. Mast cells are endowed with a palette of receptors that can recognize endogenous and exogenous products and release different sets of mediators dependent on the receptor involved. Upon recognition mast cells react by releasing mediators through one or several pathways: (1) degranulation and release of granules containing, for example, histamine, heparin, proteases, and cytokines; (2) release of newly synthesized lipid mediators such as PGD 2 , LTC 4 /D 4 /E 4 , TXA 2 and 15-­ HETE; (3) release of de novo-­ synthesized cytokines, chemokines, growth factors, and interferons; (4) release of extracellular vesicles, for example, exosomes, containing proteins, mRNA and miRNA
FIGURE 1 Mast cell activation pathways and release of mediators. Mast cells are endowed with a palette of receptors that can recognize endogenous and exogenous products and release different sets of mediators dependent on the receptor involved. Upon recognition mast cells react by releasing mediators through one or several pathways: (1) degranulation and release of granules containing, for example, histamine, heparin, proteases, and cytokines; (2) release of newly synthesized lipid mediators such as PGD 2 , LTC 4 /D 4 /E 4 , TXA 2 and 15-­ HETE; (3) release of de novo-­ synthesized cytokines, chemokines, growth factors, and interferons; (4) release of extracellular vesicles, for example, exosomes, containing proteins, mRNA and miRNACC-BY-NC-ND · From the PDF
FIGURE 2 Differential release of mediators. Depending on ligand -­ receptor interaction mast cells react by releasing different sets of mediators, those stored in granules, newly synthesized and secreted lipid mediators, and de novo produced proteins. Mast cells activated with allergen binding to IgE bound to the high-­ affinity IgE receptor, Fc ε RI, induces degranulation, secretion of lipid mediators and different types of proteins, including cytokines and chemokines. In contrast, the alarmin IL-­ 33 does not induce degranulation but causes secretion of lipid mediators, cytokines and chemokines. 185 The costimulatory molecule CD30 induces secretion of only cytokines and chemokines. 23 Viral infection leads to a variety of responses, depending on the type of virus encountered. 15 For example, respiratory syncytial virus infection induces production of type I interferons and chemokines 24
FIGURE 2 Differential release of mediators. Depending on ligand -­ receptor interaction mast cells react by releasing different sets of mediators, those stored in granules, newly synthesized and secreted lipid mediators, and de novo produced proteins. Mast cells activated with allergen binding to IgE bound to the high-­ affinity IgE receptor, Fc ε RI, induces degranulation, secretion of lipid mediators and different types of proteins, including cytokines and chemokines. In contrast, the alarmin IL-­ 33 does not induce degranulation but causes secretion of lipid mediators, cytokines and chemokines. 185 The costimulatory molecule CD30 induces secretion of only cytokines and chemokines. 23 Viral infection leads to a variety of responses, depending on the type of virus encountered. 15 For example, respiratory syncytial virus infection induces production of type I interferons and chemokines 24CC-BY-NC-ND · From the PDF
Image 4
CC-BY-NC-ND · From the PDF
Image 5
CC-BY-NC-ND · From the PDF
FIGURE 4 Models representing mast cell differentiation in hematopoiesis. (A) The tree-­ like model represents hematopoiesis as a strict series of branching events, in which cell lineage potential is lost at defined checkpoints along with differentiation from hematopoietic stem cells to lineage-­ committed cells. The position of the mast cell branch in this model is controversial. (B) The hematopoietic landscape model represents a continuum of single differentiating progenitors, in which there are multiple paths from hematopoietic stem cells to each lineage's entry point. Ba, basophil; Eo, eosinophil; Ery, erythrocyte, Gr, granulocyte(which commonly refers to basophils, eosinophils, and neutrophils), HSC, hematopoietic stem cell; Ly, lymphocyte; MC, mast cell; MK, megakaryocyte; Mo, monocyte, Neu, neutrophil
FIGURE 4 Models representing mast cell differentiation in hematopoiesis. (A) The tree-­ like model represents hematopoiesis as a strict series of branching events, in which cell lineage potential is lost at defined checkpoints along with differentiation from hematopoietic stem cells to lineage-­ committed cells. The position of the mast cell branch in this model is controversial. (B) The hematopoietic landscape model represents a continuum of single differentiating progenitors, in which there are multiple paths from hematopoietic stem cells to each lineage's entry point. Ba, basophil; Eo, eosinophil; Ery, erythrocyte, Gr, granulocyte(which commonly refers to basophils, eosinophils, and neutrophils), HSC, hematopoietic stem cell; Ly, lymphocyte; MC, mast cell; MK, megakaryocyte; Mo, monocyte, Neu, neutrophilCC-BY-NC-ND · From the PDF
Image 7
CC-BY-NC-ND · From the PDF
FIGURE 5 Fate decisions in the life of the mast cell. Mast cell progenitors (MCp) in the bone marrow (1) are entering the bloodstream and are recruited into the tissue (2). During this process, the cells have to avoid premature degranulation (2). In the tissue (3) MCs can degranulate in three possible modes, either by full exocytosis, compound exocytosis, or by kiss-­ and-­ run exocytosis
FIGURE 5 Fate decisions in the life of the mast cell. Mast cell progenitors (MCp) in the bone marrow (1) are entering the bloodstream and are recruited into the tissue (2). During this process, the cells have to avoid premature degranulation (2). In the tissue (3) MCs can degranulate in three possible modes, either by full exocytosis, compound exocytosis, or by kiss-­ and-­ run exocytosisCC-BY-NC-ND · From the PDF
Image 9
CC-BY-NC-ND · From the PDF
Image 10
CC-BY-NC-ND · From the PDF
FIGURE 6 MC-­ targeted treatments under development. Examples of treatments currently under development that target mast cell mediators, receptors, or their signaling molecules
FIGURE 6 MC-­ targeted treatments under development. Examples of treatments currently under development that target mast cell mediators, receptors, or their signaling moleculesCC-BY-NC-ND · From the PDF
Image 12
CC-BY-NC-ND · From the PDF
Image 13
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Image 14
CC-BY-NC-ND · From the PDF
FIGURE 7 Intracellular targets to inhibit MC-­ activating receptors Fc ε RI and KIT. Small molecular inhibitors that target Syk or BTK downstream of Fc ε RI inhibit the downstream signaling. The KIT-­ inhibitors target the kinase activity of the receptor. Imatinib and Nilotinib target only wild-­ type KIT, while Midostaurin and Avapritinib also target D816V-­ mutated KIT that is commonly found in systemic mastocytosis
FIGURE 7 Intracellular targets to inhibit MC-­ activating receptors Fc ε RI and KIT. Small molecular inhibitors that target Syk or BTK downstream of Fc ε RI inhibit the downstream signaling. The KIT-­ inhibitors target the kinase activity of the receptor. Imatinib and Nilotinib target only wild-­ type KIT, while Midostaurin and Avapritinib also target D816V-­ mutated KIT that is commonly found in systemic mastocytosisCC-BY-NC-ND · From the PDF
Image 16
CC-BY-NC-ND · From the PDF
Image 17
CC-BY-NC-ND · From the PDF

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Metadata

Authors
Dahlin, J. S., Maurer, M., Metcalfe, D. D., Pejler, G., Sagi‐Eisenberg, R., & Nilsson, G.
Affiliations
  • Division of Immunology and Allergy Department of Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden
  • Department of Dermatology and Allergy Dermatological Allergology Allergie‐Centrum‐Charité Charité—Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, Berlin Institute of Health Berlin Germany
  • Mast Cell Biology Section Laboratory of Allergic Diseases NIAID, NIH Bethesda MD USA
  • Department of Medical Biochemistry and Microbiology Uppsala University Uppsala Sweden
  • Department of Cell and Developmental Biology Sackler Faculty of Medicine Tel Aviv University Tel Aviv Israel
ORCID
Venue
Allergy
Publisher
Wiley
Published
2021-05-20
Volume
77
Issue
1
Pages
83-99
ISSN
  • 0105-4538
  • 1398-9995
DOI
10.1111/all.14881
Cited by
147
References
11
Language
en
Licence
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Funders
  • Cancerfonden
  • Division of Intramural Research, National Institute of Allergy and Infectious Diseases
  • Vetenskapsrådet

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Dahlin, J. S., Maurer, M., Metcalfe, D. D., Pejler, G., Sagi‐Eisenberg, R., & Nilsson, G. (2022). The ingenious mast cell: Contemporary insights into mast cell behavior and function. Allergy. https://doi.org/10.1111/all.14881