ILC2 activation by keratinocyte-derived IL-25 drives IL-13 production at sites of allergic skin inflammation

Leyva-Castillo, Juan-Manuel; Galand, C; Mashiko, Shunya; Bissonnette, Robert; McGurk, Alex; Ziegler, Steven F.; Dong, Chen; McKenzie, Andrew N. J.; Sarfati, Marika

doi:10.1016/j.jaci.2020.02.026

Cited by 80 publications

(69 citation statements)

References 50 publications

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“… 2 IL-25 acts on both ILC2 and T cells by attaching to its receptor, IL-17RB. 12 , 15 In combination with IL-33 and thymic stromal lymphopoietin, it enhances the proliferation and cytokine expression by ILC2. 12 Both IL-33 and IL-25 are highly expressed in AD lesions.…”

Section: What Causes An Increase In Infections In Ad?mentioning

confidence: 99%

The infectious complications of atopic dermatitis

Wang

Boguniewicz

et al. 2021

Annals of Allergy, Asthma & Immunology

107

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Objective Atopic dermatitis (AD) is a chronic inflammatory skin disease that is complicated by an increased risk for skin and systemic infections. Preventive therapy for AD is based on skin barrier improvement and anti-inflammatory treatments, whereas overt skin and systemic infections require antibiotics or antiviral treatments. This review updates the pathophysiology, diagnosis, management, controversy of antibiotic use, and potential treatments of infectious complications of AD. Data Sources Published literature obtained through PubMed database searches and clinical pictures. Study Selections Studies relevant to the mechanisms, diagnosis, management, and potential therapy of infectious complications of AD. Results Skin barrier defects, type 2 inflammation, Staphylococcus aureus colonization, and cutaneous dysbiosis are the major predisposing factors for the increased infections in AD. Although overt infections require antibiotics, the use of antibiotics in AD exacerbation remains controversial. Conclusion Infectious complications are a comorbidity of AD. Although not common, systemic bacterial infections and eczema herpeticum can be life-threatening. Preventive therapy of infections in AD emphasizes skin barrier improvement and anti-inflammatory therapy. The use of antibiotics in AD exacerbation requires further studies.

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Section: What Causes An Increase In Infections In Ad?mentioning

confidence: 99%

The infectious complications of atopic dermatitis

Wang

Boguniewicz

et al. 2021

Annals of Allergy, Asthma & Immunology

107

View full text Add to dashboard Cite

show abstract

“…Keratinocyte‐derived IL‐25 is involved in the induction of Th2 cells via direct activation of naive CD4 + T cells or ILC2 activation to promote innate type‐2 immune responses [50]. IL‐13 production in activated ILC2 consequently promotes TARC/CCL17‐ and macrophage‐derived chemokine (MDC)/CCL22‐mediated recruitment of Th2 cells in AD lesional skin [53]. Unlike other IL‐17 cytokine members, IL‐25 suppresses cell‐mediated immunity by preventing the development of the Th1 or Th17 immune response [50].…”

Section: Keratinocyte‐derived Cytokines Regulate Th2 Immunitymentioning

confidence: 99%

Keratinocytes: innate immune cells in atopic dermatitis

Chieosilapatham

Kiatsurayanon

Umehara

et al. 2021

Clinical and Experimental Immunology

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Summary The skin is a unique immune organ that constitutes a complex network of physical, chemical and microbiological barriers against external insults. Keratinocytes are the most abundant cell type in the epidermis. These cells form the physical skin barrier and represent the first line of the host defense system by sensing pathogens via innate immune receptors, initiating anti‐microbial responses and producing various cytokines, chemokines and anti‐microbial peptides, which are important events in immunity. A damaged epidermal barrier in atopic dermatitis allows the penetration of potential allergens and pathogens to activate keratinocytes. Among the dysregulation of immune responses in atopic dermatitis, activated keratinocytes play a role in several biological processes that contribute to the pathogenesis of atopic dermatitis. In this review, we summarize the current understanding of the innate immune functions of keratinocytes in the pathogenesis of atopic dermatitis, with a special emphasis on skin‐derived anti‐microbial peptides and atopic dermatitis‐related cytokines and chemokines in keratinocytes. An improved understanding of the innate immunity mediated by keratinocytes can provide helpful insight into the pathophysiological processes of atopic dermatitis and support new therapeutic efforts.

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“…Interleukin (IL)-4, IL-5, IL-9 and IL-13 are important cytokines that play key roles in type 2 immunity, and are usually involved in allergic diseases or during helminthic parasitic infections (8,9). Th2 cells and certain myeloid cells are considered the primary source of these type 2 cytokines (10,11); however, recent studies have reported that a rare subpopulation of innate lymphocytes are the predominant source (12)(13)(14). Type 2 innate lymphoid cells (ILC2s), which were first discovered as non-T and B cells (15,16), play a defensive role in the initial stage of helminthic infestation (17), and are considered a major component of type 2 immunity in lungs (18,19).…”

Section: Introductionmentioning

confidence: 99%

A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review)

Zhu

Lü

2021

Mol Med Rep

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Type 2 innate lymphoid cells (ILC2s) are important innate immune cells that are involved in type 2 inflammation, in both mice and humans. ILC2s are stimulated by factors, including interleukin (IL)-33 and IL-25, and activated ILC2s secrete several cytokines that mediate type 2 immunity by inducing profound changes in physiology, including activation of alternative (M2) macrophages. M2 macrophages possess immune modulatory, phagocytic, tissue repair and remodeling properties, and can regulate ILC2s under infection. The present review summarizes the role of ILC2s as innate cells and M2 macrophages as anti-inflammatory cells, and discusses current literature on their important biological significance. The present review also highlights how the crosstalk between ILC2s and M2 macrophages contributes to lung development, induces pulmonary parasitic expulsion, exacerbates pulmonary viral and fungal infections and allergic airway diseases, and promotes the development of lung diseases, such as pulmonary fibrosis, chronic obstructive pulmonary disease and carcinoma of the lungs. Contents

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ILC2 activation by keratinocyte-derived IL-25 drives IL-13 production at sites of allergic skin inflammation

Cited by 80 publications

References 50 publications

The infectious complications of atopic dermatitis

The infectious complications of atopic dermatitis

Keratinocytes: innate immune cells in atopic dermatitis

A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review)

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