ILC2 cells, or type 2 innate lymphoid cells are a type of innate lymphoid cell. They are derived from common lymphoid progenitor and belong to the lymphoid lineage. These cells lack antigen specific B or T cell receptor because of the lack of recombination activating gene. ILC2s produce type 2 cytokines (e.g. IL-4, IL-5, IL-9, IL-13).
The cell type were first described in 2001. In 2006, a similar cell population was identified in a case of helminthic infection. The name "ILC2" was not proposed until 2013. They were previously identified in literature as natural helper cells, nuocytes, or innate helper 2 cells.
ILC2s play the crucial role of secreting type 2 cytokines in response to helminth infection. They have also been implicated in the development of allergic lung inflammation. They express characteristic surface markers and receptors for chemokines, which are involved in distribution of lymphoid cells to specific organ sites. They require IL-7 for their development, which activates two transcription factors (both required by these cells)—RORα and GATA3. After stimulation with Th2 polarising cytokines (e.g. IL-25, IL-33, TSLP) ILC2s start to produce IL-5, IL-13, IL-9, IL-4. ILC2s are critical for primary responses to local Th2 antigens e.g. helmints and viruses and that is why ILC2s are abundant in tissues of skin, lungs, livers and gut.
Allergy, atopic dermatitis, and asthma
ILC2s play a variety of roles in allergy. Primarily, they provide a source of the type 2 cytokines that orchestrate the allergic immune response. They produce a profile of signals in response to pro-allergenic cytokines IL-25 and IL-33 that is similar to those produced in response to helminthic infection. Their contribution to this signaling appears to be comparable to that of T cells. In response to allergen exposure in the lungs, ILC2s produce IL-13, a necessary cytokine in the pathogenesis of allergic reactions. This response appears to be independent of T and B cells. Further, allergic responses that resemble asthma-like symptoms have been induced in mice that lack T and B cells using IL-33. It has also been found that ILC2s are present in higher concentrations in tissues where allergic symptoms are present, such as in the nasal polyps of patients with chronic rhinosinusitis and the skin from patients with atopic dermatitis.
Research identified ILC2s in adipose tissue as a factor in the development of obesity in mice. ILC2s are critical in energy homeostasis by producing methionine-enkephalin peptides in response to IL-33. This production promotes the emergence of beige adipocytes in white adipose tissue. The process of beiging leads to increased energy expenditure and decreased adiposity.
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