Type 2 Innate Lymphoid Cells: Friends or Foes—Role in Airway Allergic Inflammation and Asthma

Pishdadian, Abbas; Varasteh, Abdolreza; Sankian, Mojtaba

doi:10.1155/2012/130937

Cited by 6 publications

(3 citation statements)

References 75 publications

(114 reference statements)

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“…The mouse ILC2s were sorted from single-cell suspension of mLN or lung as Lin − sca1 + CD127 + ST2 + cells. 37 Lineage markers used are biotin-conjugated antibodies for CD3 (CD3ε, 145-2C11), CD4 (RM4-5), CD5 (53-7.3), CD8, CD19 (6D5), CD11c (HL3), CD11b (M1/70), B220 (RA3-6B2), F4/80 (BM8), Ter119, IgM (11/41), IgE (R35-72), NK1.1 (PK136), DX5 (DX5), TCRγδ (GL3), and Gr-1 (RB6-8C5). The following antibodies were also used for flow cytometry in an appropriate combination: anti-Sca-1 (D7; conjugated with PerCP-Cy5.5), anti-CD127 (A7R34; conjugated with PE or allophycocyanin (APC)), anti-c-Kit (2B8, conjugated with APC-H7), anti-ST2 (DJ8; conjugated with FITC; MD Biosciences, St Paul, MN), anti-CD287 (C398.4A; conjugated with APC), anti-KLRG1 (2F1; conjugated with FITC or PE), anti-mouse TNFR1 (55R-286; conjugated with APC), affinity purified anti-mouse DR3 (R&D Systems), donkey-anti-goat secondary antibody (PE-conjugated; Rockland Immunochemicals, Gilbertsville, PA), and Streptavidin (conjugated to FITC, PE, or APC).…”

Section: Methodsmentioning

confidence: 99%

TNF superfamily member TL1A elicits type 2 innate lymphoid cells at mucosal barriers

Yu¹,

Pappu²,

et al. 2014

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Immune responses at mucosal barriers are regulated by innate type 2 lymphoid cells (ILC2s) that elaborate effector cytokines interleukins 5 and 13 (IL5 and IL13). IL25 and IL33 are key cytokines that support ILC2s; however, mice deficient in these pathways retain some functional ILC2s. Analysis of human and murine cells revealed that ILC2s highly express tumor necrosis factor (TNF)-receptor superfamily member DR3 (TNFRSF25). Engagement of DR3 with cognate ligand TL1A promoted ILC2 expansion, survival, and function. Exogenous protein or genetic overexpression of TL1A activated ILC2s independent of IL25 or IL33. Dr3−/− mice failed to control gut helminthic infections, and failed to mount ILC2 responses in the lung after nasal challenge with papain. Our data demonstrate a key role for TL1A in promoting ILC2s at mucosal barriers.

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Section: Methodsmentioning

confidence: 99%

TNF superfamily member TL1A elicits type 2 innate lymphoid cells at mucosal barriers

Yu¹,

Pappu²,

et al. 2014

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“…ILC2s belong to one of the three subsets of ILC populations arising from common lymphoid progenitors. 56 Among ILC subsets, ILC2s are the prominent cells in the lung tissue, and upon ILC2 activation, they produce large amounts of type 2 cytokines (IL-5, IL-13, IL-9, and IL-4). 57 ILC2s influence both adaptive and innate immunity and are regarded as the counterpart of the Th2 immune pathway.…”

Section: Ilc2 In Inflammationmentioning

confidence: 99%

Group 2 innate lymphoid cells (ILC2s): The spotlight in asthma pathogenesis and lung tissue injury

Sunusi

Zhu

et al. 2021

aei

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Asthma is a heterogeneous disease with ranging etiology and severity. Asthma is a disease of chronic inflammation of the airways, with clinical symptoms of wheezing, breathlessness, cough, and chest tightness manifested as chronic fixed or variable airflow obstruction and airway hyperresponsiveness that predispose the airway epithelium to repeated injury, repair, and regeneration. In recent years, innate lymphoid cells (ILC1, ILC2, and ILC3) have been discovered. The predominant ILC type found in the lung tissue is group 2 innate lymphoid cells (ILC2s). Upon damage to the airway epithelium mediating the release of epithelial cytokines (TSLP, IL-33, and IL-25) ensued the activation of ILC2 in an antigen-independent manner. Activated ILC2 produces a significant amount of type 2 cytokines (IL-4, IL-5, IL-9, and IL-13), altogether contributing to type 2 inflammation in the airways. ILC2s are mediators of type 2 immunity for many type 2 inflammatory diseases such as asthma, since ILC2s were reported to play an important role in asthma pathogenesis. Here we discuss the role of ILC2 in the development of asthma and ILC2 effector cytokines (IL-4, IL-5, and IL-13) contributing to airway epithelial structural changes.

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“…Of interest, innate lymphoid cells (ILCs) are a heterogeneous cell population that have recently been ascribed a critical role in controlling inflammation and tissue homeostasis at mucosal sites, including the airway . Three functionally distinct subsets of ILCs have been identified: natural killer (NK) cells (cytotoxic ILCs), Rorγt+ ILCs and type 2 ILCs (ILC2).…”

Section: Hrv and The Induction Of Innate Inflammatory Responsesmentioning

confidence: 99%

Rhinoviral infection and asthma: the detection and management of rhinoviruses by airway epithelial cells

Parker

Stokes

Sabroe

2013

Clin Experimental Allergy

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Human rhinoviruses (HRV) have been linked to the development of childhood asthma and recurrent acute asthma exacerbations throughout life, and contribute considerably to the healthcare and economic burden of this disease. However, the ability of HRV infections to trigger exacerbations, and the link between allergic status and HRV responsiveness, remains incompletely understood. Whilst the receptors on human airway cells that detect and are utilized by most HRV group A and B, but not C serotypes are known, how endosomal pattern recognition receptors (PRRs) detect HRV replication products that are generated within the cytoplasm remains somewhat of an enigma. In this article, we explore a role for autophagy, a cellular homeostatic process that allows the cell to encapsulate its own cytosolic constituents, as the crucial mechanism controlling this process and regulating the innate immune response of airway epithelial cells to viral infection. We will also briefly describe some of the recent insights into the immune responses of the airway to HRV, focusing on neutrophilic inflammation that is a potentially unwanted feature of the acute response to viral infection, and the roles of IL-1 and Pellinos in the regulation of responses to HRV.

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Type 2 Innate Lymphoid Cells: Friends or Foes—Role in Airway Allergic Inflammation and Asthma

Cited by 6 publications

References 75 publications

TNF superfamily member TL1A elicits type 2 innate lymphoid cells at mucosal barriers

TNF superfamily member TL1A elicits type 2 innate lymphoid cells at mucosal barriers

Group 2 innate lymphoid cells (ILC2s): The spotlight in asthma pathogenesis and lung tissue injury

Rhinoviral infection and asthma: the detection and management of rhinoviruses by airway epithelial cells

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