Group 2 Innate Lymphoid Cells in Health and Disease

Kim, Brian; Artis, David

doi:10.1101/cshperspect.a016337

Cited by 69 publications

(58 citation statements)

References 88 publications

(164 reference statements)

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“…In humans, chronic eosinophilic rhinosinusitis with nasal polyps is associated with increased epithelial IL-33 and IL-13 + ILC2s (Shaw et al, 2013). IL-33 is expressed in skin keratinocytes and is elevated in humans and mouse models of atopic dermatitis (Kim and Artis, 2015). In mice, overexpression of IL-33 in the skin can cause atopic dermatitis-like immune pathology (Imai et al, 2013).…”

Section: Il-33 In Type 2 Immune Responsesmentioning

confidence: 99%

“…In mice, overexpression of IL-33 in the skin can cause atopic dermatitis-like immune pathology (Imai et al, 2013). The role of endogenous IL-33 in murine atopic dermatitis models has been inconsistent (Kim et al, 2013; Salimi et al, 2013), suggesting IL-33 may be one of several signals that together promote disease (Kim and Artis, 2015). IL-33 may contribute to gastrointestinal food allergy (Chu et al, 2013; Muto et al, 2014) and other eosinophilic gastrointestinal diseases, although further study is required to delineate these roles.…”

Section: Il-33 In Type 2 Immune Responsesmentioning

confidence: 99%

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Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation

2015

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Summary Interleukin-33 (IL-33) is a nuclear-associated cytokine of the IL-1 family originally described as a potent inducer of allergic type 2 immunity. IL-33 signals via the receptor ST2, which is highly expressed on group 2 innate lymphoid cells (ILC2s) and T helper 2 (Th2) cells, thus underpinning its association with helminth infection and allergic pathology. Recent studies have revealed ST2 expression on subsets of regulatory T cells, and for a role for IL-33 in tissue homeostasis and repair that suggests previously unrecognized interactions within these cellular networks. IL-33 can participate in pathologic fibrotic reactions, or, in the setting of microbial invasion, can cooperate with inflammatory cytokines to promote responses by cytotoxic NK cells, Th1 cells and CD8+ T cells. Here, we highlight the regulation and function of IL-33 and ST2, and review their roles in homeostasis, damage and inflammation, suggesting a conceptual framework for future studies.

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Section: Il-33 In Type 2 Immune Responsesmentioning

confidence: 99%

Section: Il-33 In Type 2 Immune Responsesmentioning

confidence: 99%

Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation

2015

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“…Однако в послед-ние 5 лет получены данные, позволяющие пересмо-треть концепцию Тh 2 -опосредованного генеза ал-лергического ответа. На смену Тh 2 как основной популяции иммунных клеток, опосредующих фор-мирование противопаразитарного иммунного отве-та, а также аллергии, приходят другие клетки, кото-рые по спектру продуцируемых критических цито-кинов совпадают с Тh 2 , получившие название «Group 2 innate lymphoid cells» (ILC2s) или лимфо-идные клетки врожденного иммунитета 2-го типа [15,16]. Это особые клетки, не несущие маркеров классических лимфоцитов, таких как CD3 (Т-клетки), 4 (Т-хелперы), 8 (цитотоксические Т-клетки), 19 (В-клетки) и т.д., или маркеров клеток врожденной системы иммунитета (СD14, HLA-II и другие).…”

Section: механизмы контроля целостности барьеров организма млекопитающихunclassified

“…Это особые клетки, не несущие маркеров классических лимфоцитов, таких как CD3 (Т-клетки), 4 (Т-хелперы), 8 (цитотоксические Т-клетки), 19 (В-клетки) и т.д., или маркеров клеток врожденной системы иммунитета (СD14, HLA-II и другие). С лимфоидными клетками ILC2s объеди-няет их способность в ответ на ряд факторов, о кото-рых пойдет речь ниже, синтезировать и секретиро-вать цитокины, характерные для Тh 2 : ИЛ-4, ИЛ-13 и ИЛ-5 [15,16].…”

Section: механизмы контроля целостности барьеров организма млекопитающихunclassified

The role of infection in the pathogenesis of allergodermatoses

Svirshchevskaya¹,

Matushevskaya²,

Chudakov³

et al. 2015

Klin. dermatol. venerol.

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В обзоре представлены данные зарубежных и отечественных клинических исследований по изучению роли инфекции в патогенезе аллергодерматозов и влиянию микробной флоры на течение атопического дерматита (АтД). Даны общие сведения по микрофлоре кожи: нормальная, условно-патогенная и патогенная. Показано, что микробная флора кожи у значительной части больных аллергодерматозами вызывает осложнения в течении основного заболевания. Представлены механизмы контроля целостности барьеров организма млекопитающих, в частности, отмечена роль эпидермального барьера при ассоциации АтД и инфекции. Выделены основные направления в лечении аллергодерматозов, основанные на международных и российских клинических рекомендациях по лечению АтД. Определено место топических антибактериальных и комбинированных препаратов в терапии осложненных форм аллергодерматозов. Ключевые слова: аллергодерматозы, атопический дерматит, стафилококк, лимфоидные клетки врожденного иммунитета 2-го типа, топическая терапия, комбинированная терапия, Акридерм.The review presents the data of foreign and national clinical studies on the role of infection in the pathogenesis of allergodermatoses and the influence of the microbial flora on the course of atopic dermatitis. General information on the normal, opportunistic and pathogenic microflora of the skin is provided. It is shown that the microbial flora of the skin causes complications of an underlying disease in a significant proportion of patients with allergodermatoses. The control mechanisms of the integrity of the body's barriers in mammals are presented. In particular, the role of the epidermal barrier impairment on the association of atopic dermatitis and infection is discussed. The main directions in the treatment of allergodermatoses are described based on Russian and International Clinical Guidelines for the treatment of atopic dermatisis. The significance of topical antibacterial and combined drugs in the treatment of complicated allergodermatoses is defined.

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“…ILC2 subsets may vary considerably accordingly to the anatomical location. For example, lung-resident IL-33R+ ILC2s produce IL-5 and IL-13, whereas skin ILC2s express thymic stromal lymphopoietin (TLSP) and IL-4 [188]. Indeed, vaccine adjuvants such as IL13Ra2 or IL-4R antagonist can significantly alter ILC2 function at vaccination sites, acting within the first 24 h after administration [189,190].…”

Section: Il-17-and Il-17r-related Mabs and Negative Emotions: Anxietymentioning

confidence: 99%

Therapeutic Antibody‐Based Drugs in the Treatment of Human Inflammatory Disorders

Sedger¹,

Ranasinghe²,

McDermott³

et al. 2017

Immunotherapy - Myths, Reality, Ideas, Future

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Inflammation causes debilitating human conditions and older treatments rely on global immunosuppression that non-specifically alleviates symptoms. Currently, several monoclonal antibodies (mAbs) are available that specifically block pro-inflammatory cytokines. These include mAbs specific to tumour necrosis factor (TNF), interleukin (IL)-1β,I L -6 , IL-17 and IL-12/IL-23. The chapter summarises the key elements in human inflammatory disease conditions, including various forms of arthritis, psoriasis, Crohn's disease and ulcerative colitis, plus pyrin-associated inflammatory syndromes and periodic fevers, to explain the benefit of cytokine neutralisation through mAb-type reagents. The chapter reviews the efficacy and safety of the current repertoire of anti-cytokine/cytokine receptor mAbs. It also discusses the known side effects and adverse events that are sometimes associated with systemic blockade of cytokines in vivo, and concludes that the accumulating knowledge of treatment failures can reveal unappreciated aspects of cytokine biology and even new treatment opportunities. The chapter includes mention of the rapidly expanding cohort of biosimilar mAbs and the mAbs to IL-4, IL-5 and IL-13 that are now emerging, in addition to the need for treatments for disorders that remain refractory to the current repertoire of anti-cytokine mAbs and conventional treatments. Thus, here we summarise the current status of anti-cytokine mAbs for human inflammatory diseases.

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Group 2 Innate Lymphoid Cells in Health and Disease

Cited by 69 publications

References 88 publications

Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation

Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation

The role of infection in the pathogenesis of allergodermatoses

Therapeutic Antibody‐Based Drugs in the Treatment of Human Inflammatory Disorders

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