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Lloyd, C. M., & Snelgrove, R. J. (2018). Type 2 immunity: Expanding our view. Sci. Immunol. 3(25), eaat1604. 
Added by: Dr. Enrique Feoli (28/01/2021, 21:17)   Last edited by: Dr. Enrique Feoli (11/05/2023, 20:02)
Resource type: Journal Article
DOI: 10.1126/sciimmunol.aat1604
ID no. (ISBN etc.): 2470-9468
BibTeX citation key: Lloyd2018
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Categories: BioAcyl Corp
Subcategories: Type 2 immunity
Creators: Lloyd, Snelgrove
Collection: Sci. Immunol.
Views: 1/268
Abstract
The classical vision of type 2 immune reactions is that they are characterized by a distinct cellular and cytokine repertoire that is critical for host resistance against helminthic worm infections but, when dysregulated, may cause atopic reactions that result in conditions such as asthma, rhinitis, dermatitis, and anaphylaxis. In this traditional view, the type 2 response is categorized as an adaptive immune response with differentiated T helper cells taking center stage, driving eosinophil recruitment and immunoglobulin production via the secretion of a distinct repertoire of cytokines that include interleukin-4 (IL-4), IL-5, and IL-13. The recent discovery of a group of innate cells that has the capacity to secrete copious amounts of type 2 cytokines, potentially in the absence of adaptive immunity, has reignited interest in type 2 biology. The discovery that these innate lymphoid cells and type 2 cytokines are involved in diverse biological processes—including wound healing, control of metabolic homeostasis, and temperature has considerably changed our view of type 2 responses and the cytokines, chemokines, and receptors that regulate these responses.
Added by: Dr. Enrique Feoli  Last edited by: Dr. Enrique Feoli
Notes

Fig. 2 ILC2s sense microenvironmental cues to elicit a type 2 response.

Lung-resident cells function as specialized tissue sentinels to detect a broad array of stimuli, including allergens, specific viruses, bacteria, or general host perturbations away from a homeostatic basal state. Subsequently, these sensors release a disparate set of mediators, including IL-25, TSLP, IL-33, TL1A, leukotrienes (LTs), prostaglandins (PGs), and neuropeptides VIP and NMU. These mediators converge to activate ILC2s, which produce IL-5, IL-13, and IL-9 and so function as a fundamental decision-maker in bridging tissue perturbation and induction of a TH2 response. ECM, extracellular matrix.


Added by: Dr. Enrique Feoli  Last edited by: Dr. Enrique Feoli
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