Mast cells (MCs) are tissue-resident, innate immune cells with heterogenous phenotypes imprinted by cytokines, growth factors, and other stimuli in their immediate microenvironment. Populating tissues in several waves including during fetal development, in adults bone marrow-derived progenitor cells circulate in the blood and migrate and differentiate into mature MCs in tissue. MCs are abundantly present in the skin and mucosal tissues but can be found in virtually all organs often increasing in numbers during inflammation. MCs are key effectors in IgE-associated immune responses, including allergic disorders and associated protective immune responses. They release a variety of mediators acting on immune and non-immune cells, including nerve cells, fibroblasts, endothelial cells, smooth muscle cells, and epithelial cells. MCs, via the expression of numerous other receptors, can be triggered by many other stimuli including TLR ligands, complement, and neuropeptides etc.
Playing a protective role in parasitic, bacterial, and viral infections but also venom and toxin neutralization, MCs are best known for their role in the pathogenesis of allergic diseases. Several lines of evidence have implicated MCs in the development of autoimmune diseases and a whole variety of chronic inflammatory disorders, including cardiovascular diseases, urticaria, mastocytosis, and several cancers. The manifestations of MC-driven disease are considered to be a consequence of an inappropriate activation of MC immune responses which have evolved to protect the body against a host of pathogens and perhaps toxins.
Recently, several drugs that target human MC have been developed. These include monoclonal antibodies and small molecules that can specifically inhibit MC degranulation via key receptors. The development of more effective and specific MC-altering drugs is urgently required, and existing treatment strategies should be reinvestigated to determine their potential effects on MCs. However, currently, more work is needed to develop suitable mouse models for some MC-driven diseases, and current approaches are invasive or can induce severe reactions.
In this Research Topic, we welcome the submission of Original Research, Review, Mini Review, Opinion, and Perspective articles which cover, but are not limited to, the following subtopics:
• Updates on FceRI-mediated signaling of MC
• Non-IgE mediated activation of MC
• MC development
• MC recruitment
• MC heterogeneity
• MC function in the pathogenesis of MC driven diseases
• Therapeutic targeting MC for the treatment of MC driven diseases
• Novel technologies to study MCs and understand MC driven diseases
Mast cells (MCs) are tissue-resident, innate immune cells with heterogenous phenotypes imprinted by cytokines, growth factors, and other stimuli in their immediate microenvironment. Populating tissues in several waves including during fetal development, in adults bone marrow-derived progenitor cells circulate in the blood and migrate and differentiate into mature MCs in tissue. MCs are abundantly present in the skin and mucosal tissues but can be found in virtually all organs often increasing in numbers during inflammation. MCs are key effectors in IgE-associated immune responses, including allergic disorders and associated protective immune responses. They release a variety of mediators acting on immune and non-immune cells, including nerve cells, fibroblasts, endothelial cells, smooth muscle cells, and epithelial cells. MCs, via the expression of numerous other receptors, can be triggered by many other stimuli including TLR ligands, complement, and neuropeptides etc.
Playing a protective role in parasitic, bacterial, and viral infections but also venom and toxin neutralization, MCs are best known for their role in the pathogenesis of allergic diseases. Several lines of evidence have implicated MCs in the development of autoimmune diseases and a whole variety of chronic inflammatory disorders, including cardiovascular diseases, urticaria, mastocytosis, and several cancers. The manifestations of MC-driven disease are considered to be a consequence of an inappropriate activation of MC immune responses which have evolved to protect the body against a host of pathogens and perhaps toxins.
Recently, several drugs that target human MC have been developed. These include monoclonal antibodies and small molecules that can specifically inhibit MC degranulation via key receptors. The development of more effective and specific MC-altering drugs is urgently required, and existing treatment strategies should be reinvestigated to determine their potential effects on MCs. However, currently, more work is needed to develop suitable mouse models for some MC-driven diseases, and current approaches are invasive or can induce severe reactions.
In this Research Topic, we welcome the submission of Original Research, Review, Mini Review, Opinion, and Perspective articles which cover, but are not limited to, the following subtopics:
• Updates on FceRI-mediated signaling of MC
• Non-IgE mediated activation of MC
• MC development
• MC recruitment
• MC heterogeneity
• MC function in the pathogenesis of MC driven diseases
• Therapeutic targeting MC for the treatment of MC driven diseases
• Novel technologies to study MCs and understand MC driven diseases
