Interleukin‐33 (<scp>IL</scp>‐33): A nuclear cytokine from the <scp>IL</scp>‐1 family

Cayrol, Corinne; Girard, Jean-Philippe

doi:10.1111/imr.12619

Cited by 652 publications

(655 citation statements)

References 152 publications

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“…Interestingly, homeostatic signaling via the IL‐33/ST2 ( IL1rl1 ) axis, which is usually associated with tissue damage, appears to balance and adjust the degree of T‐cell anergy in the neonatal host . Also, the induction of peripheral tolerance to self‐antigen may have to precede the tolerance to microbial and dietary antigens at mucosal sites .…”

Section: Towards the Concept Of A Temporally Layered Postnatal Establmentioning

confidence: 99%

‘Layered immunity’ and the ‘neonatal window of opportunity’ – timed succession of non‐redundant phases to establish mucosal host–microbial homeostasis after birth

Hornef

Torow

2019

Immunology

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Summary The intricate host–microbial interaction and the overwhelming complexity of the mucosal immune system in the adult host raise the question of how this system is initially established. Here, we propose the implementation of the concept of the ‘postnatal window of opportunity’ into the model of a ‘layered immunity’ to explain how the newborn's mucosal immune system matures and how host–microbial immune homeostasis is established after birth. We outline the concept of a timed succession of non‐redundant phases during postnatal immune development and discuss the possible influence of external factors and conditions.

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Section: Towards the Concept Of A Temporally Layered Postnatal Establmentioning

confidence: 99%

‘Layered immunity’ and the ‘neonatal window of opportunity’ – timed succession of non‐redundant phases to establish mucosal host–microbial homeostasis after birth

Hornef

Torow

2019

Immunology

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“…While the role of MCs is well established, the functional significance of basophils has recently gained attention. Both mast cells and basophils express high-affinity IgE receptor (FcεR1) and ST2 on their surfaces and are activated by IgE cross-linking as well as IL-33 [23]. Interestingly, mast cells are resident tissue based, but basophils are blood-borne and often recruited to tissues where they attain final activation status.…”

Section: Introductionmentioning

confidence: 99%

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

Kuruvilla

Lee

2018

Clinic Rev Allerg Immunol

775

719

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The model of asthma as a single entity has now been replaced by a much more complex biological network of distinct and interrelating inflammatory pathways. The term asthma is now considered an umbrella diagnosis for several diseases with distinct mechanistic pathways (endotypes) and variable clinical presentations (phenotypes). The precise definition of these endotypes is central to asthma management due to inherent therapeutic and prognostic implications. This review presents the molecular mechanisms behind the heterogeneity of airway inflammation in asthmatic patients. Asthma endotypes may be broadly regarded as type 2 (T2) high or T2-low. Several biologic agents have been approved for T2-high asthma, with numerous other therapeutics that are incipient and similarly targeted at specific molecular mechanisms. Collectively, these advances have shifted existing paradigms in the approach to asthma to tailor novel therapies.

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“…Interleukin (IL)-33 is a member of the IL-1 cytokine family [5, 6] and is expressed in many organs and cell types, such as dendritic cells [7], macrophages [8], epithelial cells [9], endothelial cells [10]. ST2 is an IL-33 receptor encoded by the IL1RL1 gene and has a soluble form (sST2) and a membrane-anchored form (ST2L) [11].…”

Section: Introductionmentioning

confidence: 99%

IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma

et al. 2019

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Background: Melanoma, an extremely malignant form of cancer, poses a significant health risk. Vasculogenic mimicry (VM), blood vessels formed by tumor cells instead of endothelial cells, is an important factor for the rapid progression of melanoma. Interleukin (IL)-33 is an inflammatory factor commonly found in the tumor microenvironment and plays an important role in the progression of many tumors. IL-33 acts on immune cells and tumor cells through its receptor ST2. This study hypothesized that IL-33 directly affects the progression of melanoma. Objectives: This study was designed to investigate the effect of IL-33 on VM of melanoma and its potential mechanism of action. Methods: The expression of ST2 was evaluated in 66 cases of melanoma collected from human patients, and the differences were analyzed. In vitro experiments were conducted to study the effects of the IL-33/ST2 axis on cell migration and invasion and to elucidate possible mechanisms. Results: ST2 expression is associated with that of matrix metalloproteinase (MMP)-2 and VM in melanoma of patients. IL-33 increases the abilities of proliferation, migration and invasion of melanoma cells and VM tube formation through ST2. IL-33 induces the production of MMP-2/9 via ERK1/2 phosphorylation. Conclusion: IL-33 can directly act on melanoma cells and promote its development.

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Interleukin‐33 (IL‐33): A nuclear cytokine from the IL‐1 family

Abstract: SummaryInterleukin-33 (IL-33) is a tissue-derived nuclear cytokine from the IL-1 family abun- K E Y W O R D Sallergy, cytokine, IL-33, ILC2, inflammation, innate immunity

Cited by 652 publications

References 152 publications

‘Layered immunity’ and the ‘neonatal window of opportunity’ – timed succession of non‐redundant phases to establish mucosal host–microbial homeostasis after birth

‘Layered immunity’ and the ‘neonatal window of opportunity’ – timed succession of non‐redundant phases to establish mucosal host–microbial homeostasis after birth

Understanding Asthma Phenotypes, Endotypes, and Mechanisms of Disease

IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma

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