Role of myeloid cells in the regulation of group 2 innate lymphoid cell‐mediated allergic inflammation

Lei, Aihua; He, Yumei; Yang, Qiong; Li, Xiaofang; Li, Ranhui

doi:10.1111/imm.13232

Cited by 7 publications

(3 citation statements)

References 85 publications

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“…Unlike Th2 cells, they lack T cell receptor (TCR) and cannot recognize antigen. In response to epithelial-derived cytokines, such as IL-25 and IL-33, they produce large amounts of IL-5, IL-9, and IL-13 (134). Recent findings indicate that in addition to being primed by epithelial cellderived cytokines, ILC2s can also be activated in a mast cell driven manner, and conversely that effects of ILC2s on mast cells can influence the severity of anaphylaxis in food allergy.…”

Section: Mast Cells Basophils Ilc2s and Ige Antibodies Act As Adjumentioning

confidence: 99%

IgE and IgG Antibodies as Regulators of Mast Cell and Basophil Functions in Food Allergy

et al. 2020

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Food allergy is a major health issue, affecting the lives of 8% of U.S. children and their families. There is an urgent need to identify the environmental and endogenous signals that induce and sustain allergic responses to ingested allergens. Acute reactions to foods are triggered by the activation of mast cells and basophils, both of which release inflammatory mediators that lead to a range of clinical manifestations, including gastrointestinal, cutaneous, and respiratory reactions as well as systemic anaphylaxis. Both of these innate effector cell types express the high affinity IgE receptor, FcϵRI, on their surface and are armed for adaptive antigen recognition by very-tightly bound IgE antibodies which, when cross-linked by polyvalent allergen, trigger degranulation. These cells also express inhibitory receptors, including the IgG Fc receptor, FcγRIIb, that suppress their IgE-mediated activation. Recent studies have shown that natural resolution of food allergies is associated with increasing food-specific IgG levels. Furthermore, oral immunotherapy, the sequential administration of incrementally increasing doses of food allergen, is accompanied by the strong induction of allergen-specific IgG antibodies in both human subjects and murine models. These can deliver inhibitory signals via FcγRIIb that block IgE-induced immediate food reactions. In addition to their role in mediating immediate hypersensitivity reactions, mast cells and basophils serve separate but critical functions as adjuvants for type 2 immunity in food allergy. Mast cells and basophils, activated by IgE, are key sources of IL-4 that tilts the immune balance away from tolerance and towards type 2 immunity by promoting the induction of Th2 cells along with the innate effectors of type 2 immunity, ILC2s, while suppressing the development of regulatory T cells and driving their subversion to a pathogenic pro-Th2 phenotype. This adjuvant effect of mast cells and basophils is suppressed when inhibitory signals are delivered by IgG antibodies signaling via FcγRIIb. This review summarizes current understanding of the immunoregulatory effects of mast cells and basophils and how these functions are modulated by IgE and IgG antibodies. Understanding these pathways could provide important insights into innovative strategies for preventing and/or reversing food allergy in patients.

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Section: Mast Cells Basophils Ilc2s and Ige Antibodies Act As Adjumentioning

confidence: 99%

IgE and IgG Antibodies as Regulators of Mast Cell and Basophil Functions in Food Allergy

et al. 2020

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“…Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) as a subpopulation of neutrophils are necessary for ILC2 function to be effectively suppressed. Therefore, increasing PMN-MDSCs might be helpful for controlling ILC2-driven AD [228,229].…”

Section: Neutrophil Heterogeneitymentioning

confidence: 99%

Neutrophils in Inflammatory Diseases: Unraveling the Impact of Their Derived Molecules and Heterogeneity

Riaz,

Sohn

2023

Cells

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Inflammatory diseases involve numerous disorders and medical conditions defined by an insufficient level of self-tolerance. These diseases evolve over the course of a multi-step process through which environmental variables play a crucial role in the emergence of aberrant innate and adaptive immunological responses. According to experimental data accumulated over the past decade, neutrophils play a significant role as effector cells in innate immunity. However, neutrophils are also involved in the progression of numerous diseases through participation in the onset and maintenance of immune-mediated dysregulation by releasing neutrophil-derived molecules and forming neutrophil extracellular traps, ultimately causing destruction of tissues. Additionally, neutrophils have a wide variety of functional heterogeneity with adverse effects on inflammatory diseases. However, the complicated role of neutrophil biology and its heterogeneity in inflammatory diseases remains unclear. Moreover, neutrophils are considered an intriguing target of interventional therapies due to their multifaceted role in a number of diseases. Several approaches have been developed to therapeutically target neutrophils, involving strategies to improve neutrophil function, with various compounds and inhibitors currently undergoing clinical trials, although challenges and contradictions in the field persist. This review outlines the current literature on roles of neutrophils, neutrophil-derived molecules, and neutrophil heterogeneity in the pathogenesis of autoimmune and inflammatory diseases with potential future therapeutic strategies.

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“…Besides, TSLP; and IL- 9 activate STAT5 and induce ILC2 survival. IL-4, IL-9, and IL-10 also work on ILC2s in an autocrine manner to maintain cytokine secretion, forming a positive feedback loop ( 193 – 195 ).…”

Section: The Crosstalk Of Immune Cells In Csumentioning

confidence: 99%

The Role of Crosstalk of Immune Cells in Pathogenesis of Chronic Spontaneous Urticaria

Zhou

et al. 2022

Front. Immunol.

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Chronic spontaneous urticaria (CSU) is defined as recurrent episodes of spontaneous wheal development and/or angioedema for more than six weeks and at least twice a week. The core link in the pathogenesis of CSU is the activation of mast cells, T cells, eosinophils, and other immune cells infiltrating around the small venules of the lesion. Increased vascular permeability, vasodilatation, and recruitment of inflammatory cells directly depend on mast cell mediators’ release. Complex regulatory systems tightly influence the critical roles of mast cells in the local microenvironment. The bias toward Th2 inflammation and autoantibodies derived from B cells, histamine expressed by basophils, and initiation of the extrinsic coagulation pathway by eosinophils or monocytes exerts powerful modulatory influences on mast cells. Cell-to-cell interactions between mast cells and eosinophils/T cells also are regulators of their function and may involve CSU’s pathomechanism. This review summarizes up-to-date knowledge regarding the crosstalk between mast cells and other immune cells, providing the impetus to develop new research concepts and treatment strategies for CSU.

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Role of myeloid cells in the regulation of group 2 innate lymphoid cell‐mediated allergic inflammation

Abstract: Myeloid cells, by producing inflammatory mediators, play an important role in regulating ILC2‐driven allergic inflammation.

Cited by 7 publications

References 85 publications

IgE and IgG Antibodies as Regulators of Mast Cell and Basophil Functions in Food Allergy

IgE and IgG Antibodies as Regulators of Mast Cell and Basophil Functions in Food Allergy

Neutrophils in Inflammatory Diseases: Unraveling the Impact of Their Derived Molecules and Heterogeneity

The Role of Crosstalk of Immune Cells in Pathogenesis of Chronic Spontaneous Urticaria

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