scholarly journals Group 2 innate lymphoid cells license dendritic cells to potentiate memory TH2 cell responses

2015 ◽  
Vol 17 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Timotheus Y F Halim ◽  
You Yi Hwang ◽  
Seth T Scanlon ◽  
Habib Zaghouani ◽  
Natalio Garbi ◽  
...  
2014 ◽  
Vol 192 (5) ◽  
pp. 2442-2448 ◽  
Author(s):  
Ananda S. Mirchandani ◽  
Anne-Gaelle Besnard ◽  
Edwin Yip ◽  
Charlotte Scott ◽  
Calum C. Bain ◽  
...  

Rheumatology ◽  
2019 ◽  
Vol 58 (10) ◽  
pp. 1740-1745 ◽  
Author(s):  
Sofie L M Blokland ◽  
Lucas L van den Hoogen ◽  
Emmerik F A Leijten ◽  
Sarita A Y Hartgring ◽  
Ruth Fritsch ◽  
...  

Abstract Objective The role of innate lymphoid cells (ILCs) in the pathophysiology of rheumatic diseases is emerging. Evidence from animal studies implicate type I IFN, produced by plasmacytoid dendritic cells, to be involved in regulating the survival of group 2 and group 3 ILCs (ILC2s and ILC3s) via the upregulation of Fas (CD95) expression. For the first time, we explored the frequency and phenotype of circulating ILCs in SLE and primary Sjögren’s syndrome (pSS) in relationship to the IFN signature. Methods Frequencies and phenotypes of ILC subsets and plasmacytoid dendritic cells were assessed by flow cytometry in peripheral blood of patients with SLE (n = 20), pSS (n = 20) and healthy controls (n = 17). Patients were stratified by the presence or absence of an IFN signature as assessed by RT-qPCR on circulating mononuclear cells. Results ILC1 frequencies were increased in peripheral blood of patients with SLE as compared with healthy controls and correlate with disease activity in pSS patients. Overall, the frequencies of ILC2s or ILC3s did not differ between patients with SLE, pSS and healthy controls. However, patients with a high type I IFN signature expressed elevated levels of Fas on ILC2s and ILC3s, which coincided with decreased frequencies of these cells in blood. Conclusion The presence of a type I IFN signature is related to Fas expression and frequencies of circulating ILC2s and ILC3s in patients with SLE and pSS, potentially altering the homeostatic balance of ILCs.


Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3452
Author(s):  
Enrico Maggi ◽  
Irene Veneziani ◽  
Lorenzo Moretta ◽  
Lorenzo Cosmi ◽  
Francesco Annunziato

Group 2 Innate Lymphoid Cells (ILC2s) belong to the family of helper ILCs which provide host defense against infectious agents, participate in inflammatory responses and mediate lymphoid organogenesis and tissue repair, mainly at the skin and mucosal level. Based on their transcriptional, phenotypic and functional profile, ILC2s mirror the features of the adaptive CD4+ Th2 cell subset, both contributing to the so-called type 2 immune response. Similar to other ILCs, ILC2s are rapidly activated by signals deriving from tissue and/or other tissue-resident immune cells. The biologic activity of ILCs needs to be tightly regulated in order to prevent them from contributing to severe inflammation and damage in several organs. Indeed, ILC2s display both enhancing and regulatory roles in several pathophysiological conditions, including tumors. In this review, we summarize the actual knowledge about ILC2s ability to induce or impair a protective immune response, their pro- or antitumor activity in murine models, human (children and adults) pathologies and the potential strategies to improve cancer immunotherapy by exploiting the features of ILC2s.


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