Introduction to “allergic inflammation”

Nakayama, Toshinori

doi:10.1111/imr.12566

Cited by 14 publications

(13 citation statements)

References 33 publications

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“…Allergen-specific CD4 + T helper type 2 (Th2) cells are pivotal players in causing and maintaining the allergic diseases as they specifically recognize the allergen and induce the subsequent development of allergic inflammation (16)(17)(18). DCs are essential antigen-presenting cells (APCs) that initiate immunity by stimulating and differentiating antigen-specific naive T cells (1,19).…”

Section: Introductionmentioning

confidence: 99%

Granulocyte Macrophage-Colony Stimulating Factor Produces a Splenic Subset of Monocyte-Derived Dendritic Cells That Efficiently Polarize T Helper Type 2 Cells in Response to Blood-Borne Antigen

et al. 2022

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Dendritic cells (DCs) are key antigen-presenting cells that prime naive T cells and initiate adaptive immunity. Although the genetic deficiency and transgenic overexpression of granulocyte macrophage-colony stimulating factor (GM-CSF) signaling were reported to influence the homeostasis of DCs, the in vivo development of DC subsets following injection of GM-CSF has not been analyzed in detail. Among the treatment of mice with different hematopoietic cytokines, only GM-CSF generates a distinct subset of XCR1-33D1- DCs which make up the majority of DCs in the spleen after three daily injections. These GM-CSF-induced DCs (GMiDCs) are distinguished from classical DCs (cDCs) in the spleen by their expression of CD115 and CD301b and by their superior ability to present blood-borne antigen and thus to stimulate CD4+ T cells. Unlike cDCs in the spleen, GMiDCs are exceptionally effective to polarize and expand T helper type 2 (Th2) cells and able to induce allergic sensitization in response to blood-borne antigen. Single-cell RNA sequencing analysis and adoptive cell transfer assay reveal the sequential differentiation of classical monocytes into pre-GMiDCs and GMiDCs. Interestingly, mixed bone marrow chimeric mice of Csf2rb+/+ and Csf2rb-/- demonstrate that the generation of GMiDCs necessitates the cis expression of GM-CSF receptor. Besides the spleen, GMiDCs are generated in the CCR7-independent resident DCs of the LNs and in some peripheral tissues with GM-CSF treatment. Also, small but significant numbers of GMiDCs are generated in the spleen and other tissues during chronic allergic inflammation. Collectively, our present study identifies a splenic subset of CD115hiCD301b+ GMiDCs that possess a strong capacity to promote Th2 polarization and allergic sensitization against blood-borne antigen.

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Section: Introductionmentioning

confidence: 99%

Granulocyte Macrophage-Colony Stimulating Factor Produces a Splenic Subset of Monocyte-Derived Dendritic Cells That Efficiently Polarize T Helper Type 2 Cells in Response to Blood-Borne Antigen

et al. 2022

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“…Allergic diseases in the upper and lower airways include asthma, allergic rhinitis, and nasal polyposis. In airway allergic reactions, antigens that have penetrated epithelial layers are engulfed by dendritic cells (DCs), inducing them to mature and migrate to the lymph nodes, where they activate naïve T cells into effecter T helper 2 (Th2) cells [6]. Cytokines such as interleukin-4 (IL-4), IL-5, and IL-13 are released from Th2 cells or type 2 innate lymphoid (ILC2) cells.…”

Section: Introductionmentioning

confidence: 99%

The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy

Lee

Kim

2020

IJMS

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Prostaglandins (PGs) are a family of lipid compounds that are derived from arachidonic acid via the cyclooxygenase pathway, and consist of PGD 2 , PGI 2 , PGE 2 , PGF 2 , and thromboxane B 2 . PGs signal through G-protein coupled receptors, and individual PGs affect allergic inflammation through different mechanisms according to the receptors with which they are associated. In this review article, we have focused on the metabolism of the cyclooxygenase pathway, and the distinct biological effect of each PG type on various cell types involved in allergic airway diseases, including asthma, allergic rhinitis, nasal polyposis, and aspirin-exacerbated respiratory disease.

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“…Furthermore, several recent findings suggested that ILC2 play an important role in eosinophilic airway inflammation in mice that lack the ability to mount adaptive immune responses 14 , 15 . Th2 cells and ILC2 may contribute to distinct types of inflammation such as allergen-specific and non-specific allergic inflammation, respectively 16 . Th2 cells and ILC2s are the major source of Th2 cytokines in allergic asthma, and these cells may also collaborate in allergen-driven innate and adaptive type2-lung inflammation 17 , 18 .…”

Section: Introductionmentioning

confidence: 99%

DUSP10 constrains innate IL-33-mediated cytokine production in ST2hi memory-type pathogenic Th2 cells

et al. 2018

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ST2hi memory-type Th2 cells are identified as a pathogenic subpopulation in eosinophilic airway inflammation. These ST2hi pathogenic Th2 cells produce large amount of IL-5 upon T cell receptor stimulation, but not in response to IL-33 treatment. By contrast, IL-33 alone induces cytokine production in ST2+ group 2 innate lymphoid cells (ILC2). Here we show that a MAPK phosphatase Dusp10 is a key negative regulator of IL-33-induced cytokine production in Th2 cells. In this regard, Dusp10 is expressed by ST2hi pathogenic Th2 cells but not by ILC2, and Dusp10 expression inhibits IL-33-induced cytokine production. Mechanistically, this inhibition is mediated by DUSP10-mediated dephosphorylation and inactivation of p38 MAPK, resulting in reduced GATA3 activity. The deletion of Dusp10 renders ST2hi Th2 cells capable of producing IL-5 by IL-33 stimulation. Our data thus suggest that DUSP10 restricts IL-33-induced cytokine production in ST2hi pathogenic Th2 cells by controlling p38-GATA3 activity.

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Introduction to “allergic inflammation”

Abstract: Allergic inflammation is a hallmark of pathology of type 2 inflammatory disorders, such as asthma, atopic dermatitis, rhinosinusitis, and food allergy. Eosinophilic inflammation and IgE-mediated hyperre-

Cited by 14 publications

References 33 publications

Granulocyte Macrophage-Colony Stimulating Factor Produces a Splenic Subset of Monocyte-Derived Dendritic Cells That Efficiently Polarize T Helper Type 2 Cells in Response to Blood-Borne Antigen

Granulocyte Macrophage-Colony Stimulating Factor Produces a Splenic Subset of Monocyte-Derived Dendritic Cells That Efficiently Polarize T Helper Type 2 Cells in Response to Blood-Borne Antigen

The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy

DUSP10 constrains innate IL-33-mediated cytokine production in ST2hi memory-type pathogenic Th2 cells

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