IL-33, IL-25, and TSLP induce a distinct phenotypic and activation profile in human type 2 innate lymphoid cells

Camelo, Ana Paula; Rosignoli, Guglielmo; Ohne, Yoichiro; Stewart, Ross; Overed-Sayer, Catherine; Sleeman, Matthew A.; May, Richard

doi:10.1182/bloodadvances.2016002352

Cited by 141 publications

(145 citation statements)

References 40 publications

(48 reference statements)

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“…75 TSLP is important for ILC2s survival, while ILC2s activation is more dependent on IL-33. 76 IL-33 has been demonstrated to drive IL-13 production from ILC2s in CRSwNP. 77 TSLP-activated dendritic cells (DCs) have been shown to preferentially drive Th2 cell differentiation in an OX40L-dependent manner.…”

Section: Epithelial Barrier Defect and Reduced Innate Immunity In Crsmentioning

confidence: 98%

Pathophysiologic mechanisms of chronic rhinosinusitis and their roles in emerging disease endotypes

Cao

Wang

Schleimer

et al. 2019

Annals of Allergy, Asthma & Immunology

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Objective: Chronic rhinosinusitis (CRS) is a heterogeneous disorder with distinct pathophysiologic mechanisms. Based on the transcription factor expression and cytokine production patterns in different types of innate lymphoid cells (ILCs), in parallel with those of adaptive CD4+ T helper (Th) cells and CD8+ cytotoxic T (Tc) cells, new perspectives on endotypes of patients are emerging around the immune response deviation into type 1 (orchestrated by ILC1s, Tc1 and Th1 cells), type 2 (characterized by ILC2s, Tc2 and Th2 cells), and type 3 (mediated by ILC3s, Tc17 and Th17 cells) responses. Additionally, cluster analysis has been applied to the endotyping of CRS in recent years, which has provided additional novel insights into the CRS pathogenesis. This article aims to review pathological mechanisms of CRS on the basis of type 1, type 2, and type 3 immune responses and how they inform us to begin to understand CRS endotypes. This article also reviews the recent cluster analysis studies of CRS endotypes. Finally, the impact of endotype on therapeutic management of CRS is summarized. Data Sources: Review of published literature. Study Selections: Relevant literature concerning CRS endotypes and the possible underlying mechanisms were obtained from a PubMed search and summarized here. Results and Conclusion: Both CRSwNP and CRSsNP are comprised of distinct endotypes with distinct deviated immune responses, pathogenic mechanisms, and different responses to medical and surgical treatment. An endotype of CRS with prominent type 2 immune responses is the most well studied endotype, and generally can benefit from treatment with steroids and specific type 2 disrupting biologics.

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Section: Epithelial Barrier Defect and Reduced Innate Immunity In Crsmentioning

confidence: 98%

Pathophysiologic mechanisms of chronic rhinosinusitis and their roles in emerging disease endotypes

Cao

Wang

Schleimer

et al. 2019

Annals of Allergy, Asthma & Immunology

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“…Beyond their respective dichotomy in cytokine production, ILC2 cells and ILC3 cells can produce several common cytokines. Both subsets are able to produce IL‐8 and granulocyte–macrophage colony‐stimulating factor (GM‐CSF) after activation . Whereas IL‐8 is a chemokine capable of recruiting neutrophils, GM‐CSF can induce dendritic cell maturation, survival and activation of macrophages, neutrophils and eosinophils.…”

Section: Groups 2 and 3 Ilcs: More Than Th2‐ And Th17‐like Cell Populmentioning

confidence: 99%

Dissecting human ILC heterogeneity: more than just three subsets

Simoni

Newell

2017

Immunology

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SummaryInnate lymphoid cells (ILCs) have been divided into three distinct groups based on functional capacities, cytokine profiles and transcription factor expression. Studies performed mainly in mice have demonstrated the importance of ILCs in chronic inflammation, infection, allergy and cancer. In this review, we discuss the heterogeneity of human ILC and focus primarily on the taxonomy of human ILC cell subsets and their phenotypical and functional diversity. We summarize recent findings concerning the diversity of ILCs between and within the major subsets [natural killer (NK), ILC1, intra-epithelial ILC1 (ieILC1), ILC2, ILC3, lymphoid tissues inducer (LTi) and ILC progenitor (ILCP)], as well as the abundance of each in human tissues. We also discuss the similarities observed between groups of cells in term of receptors expressed and cytokines produced, and how these relate to the pleiotropic properties of each subset.

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“…77–79 In vitro stimulation of human ILC2 increases the expression of the receptors for IL-25, IL-33, and TSLP, suggesting similar feed-forward loops may boost ILC2 responses in humans. 80 In addition, ILC2 but not CD4 + Th2 cells exhibit corticosteroid resistance in both mice and humans, particularly when they are stimulated by TSLP, suggesting ILC2 as pathophysiologic mediators in corticosteroid-resistant asthma. 81–84 …”

Section: Ilc2 Mechanisms Of Pathogenesis In Allergic Diseasementioning

confidence: 98%