Overexpression of Notch ligand Delta-like-1 by dendritic cells enhances their immunoregulatory capacity and exerts antiallergic effects on Th2-mediated allergic asthma in mice

Lee, Chen Chen; Lin, Chu Lun; Leu, Sy Jye; Lee, Yueh Lun

doi:10.1016/j.clim.2017.10.005

Cited by 21 publications

(13 citation statements)

References 52 publications

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“…Immature DCs constitutively express Jagged-1, which induced TH2 polarization in CD4 + T cells while DC-specific Jagged-1 depletion inhibited Th2 polarization [56]. Overexpression of Notch ligand Delta-1 in DCs exerted anti-allergic effects on Th2-mediated allergic asthma in mice [57]. This result supports a previous report that up-regulation of Notch ligands Delta-1 and Delta-4 in DCs inhibits Th2 development via the MyD88-dependent pathway [55].…”

Section: Dc-mediated Th2 Immunitysupporting

confidence: 85%

“…However, the results obtained from an animal model must be interpreted with caution, as they may not be applicable to human immune diseases. Diseases associated with Th2 dysfunction include Omenn syndrome [97], asthma [57,98,99], AD [100][101][102], progressive systemic sclerosis [103], cryptogenic fibrosing alveolitis [104], chronic periodontitis [105], progression to AIDS in HIV infection [106], and tumor progression [107].…”

Section: Diseases Associated With Dc-mediated Th2 Immunitymentioning

confidence: 99%

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Dendritic Cell-Mediated Th2 Immunity and Immune Disorders

Kumar¹,

Ashraf²,

Jeong³

et al. 2019

Preprint

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Dendritic cells (DCs) are the professional antigen-presenting cells that recognize and present antigens to naïve T cells to induce antigen-specific adaptive immunity. Among the T-cell subsets, T helper type 2 (Th2) cells produce the humoral immune responses required for protection against helminthic disease by activating B cells. DCs induce a Th2 immune response at a certain immune environment. Basophil, eosinophil, mast cells, and type 2 innate lymphoid cells also induce Th2 immunity. However, in the case of DCs, controversy remains regarding which subsets of DCs induce Th2 immunity, which genes in DCs are directly or indirectly involved in inducing Th2 immunity, and the detailed mechanisms underlying induction, regulation, or maintenance of the DC-mediated Th2 immunity against allergic environments and parasite infection. A recent study has shown that a genetic defect in DCs causes an enhanced Th2 immunity leading to a severe atopic dermatitis. We summarize the Th2 immune-inducing DC subsets, the genetic and environmental factors which involved in DC-mediated Th2 immunity, and current therapeutic approaches for Th2-mediated immune disorders. This review is to provide an improved understanding of DC-mediated Th2 immunity and Th1/Th2 immune balancing, leading to control over their adverse consequences.

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Section: Dc-mediated Th2 Immunitysupporting

confidence: 85%

Section: Diseases Associated With Dc-mediated Th2 Immunitymentioning

confidence: 99%

Dendritic Cell-Mediated Th2 Immunity and Immune Disorders

Kumar¹,

Ashraf²,

Jeong³

et al. 2019

Preprint

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“…Moreover, ILC-2-derived IL-13 facilitates the migration of activated lung CD11b + cDCs to the draining mediastinal lymph nodes (LNs), where they induce Th2 responses [17]. Immature DCs after uptaking the inhaled antigens become mature and migrate to regional LNs to present antigens to naïve T cells which results in differentiation of CD4+ T cells into Th2 cells involved in allergic asthma [31]. Interestingly, some helper T cells capable of producing IL-21 adopt a follicular helper T cell (T FH ) subset [17].…”

Section: Innate Immune Cells In Asthma (Recruitment and Function)mentioning

confidence: 99%

Mast Cell-Mediated Orchestration of the Immune Responses in Human Allergic Asthma: Current Insights

Komi

Bjermer

2018

Clinic Rev Allerg Immunol

100

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Improving the lung function after experimental allergen challenge by blocking of mast cell (MC) mediators and the capability of MC mediators (including histamine, prostaglandin (PG) D2, and leukotriene (LT) C4) in induction of mucosal edema, bronchoconstriction, and mucus secretion provide evidence that MCs play a key role in pathophysiology of asthma. In asthma, the number of MCs increases in the airways and infiltration of MCs in a variety of anatomical sites including the epithelium, the submucosal glands, and the smooth muscle bundles occurs. MC localization within the ASM is accompanied with the hypertrophy and hyperplasia of the layer, and smooth muscle dysfunction that is mainly observed in forms of bronchial hyperresponsiveness, and variable airflow obstruction. Owing to the expression of a wide range of surface receptors and releasing various cytoplasmic mediators, MCs orchestrate the pathologic events of the disease. MC-released preformed mediators including chymase, tryptase, and histamine and de novo synthesized mediators such as PGD2, LTC4, and LTE4 in addition of cytokines mainly TGFβ1, TSLP, IL-33, IL-4, and IL-13 participate in pathogenesis of asthma. The release of MC mediators and MC/airway cell interactions during remodeling phase of asthma results in persistent cellular and structural changes in the airway wall mainly epithelial cell shedding, goblet cell hyperplasia, hypertrophy of ASM bundles, fibrosis in subepithelial region, abnormal deposition of extracellular matrix (ECM), increased tissue vascularity, and basement membrane thickening. We will review the current knowledge regarding the participation of MCs in each stage of asthma pathophysiology including the releasing mediators and their mechanism of action, expression of receptors by which they respond to stimuli, and finally the pharmaceutical products designed based on the strategy of blocking MC activation and mediator release.

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“…9 For immunotherapeutic treatment of allergic asthma, our previous study reported that DCs transduced with the DLL1 gene by adenoviruses possess the ability to promote Th1 cell development. 8 Additionally, we proved that Ad-Jagged1-infected DCs enhance the generation of Foxp3 + Treg cells. 10 Herein, we further demonstrated that Ad-DLL4-infected DCs promoted the development of Th1 cells and exerted an immunotherapeutic effect by altering the Th1/Th2 cell ratio.…”

mentioning

confidence: 71%

“…Previous studies have shown that IL-4 induces IgE production and that IFN-γ drives IgG 2a secretion. 8 In the PC group, a high level of IgE and a low level of IgG 2a production were observed (Fig. 1h).…”

mentioning

confidence: 85%