ILC2s have been primarily identified at environmental-mucosal interfaces and can be activated quickly by environmental antigens and pathogens to produce large quantities of IL-5 and IL-13. As a result of the production of these cytokines, ILC2s have been implicated in the host response to allergens, viruses, and parasites. However, the exact role of ILC2s in any human disease state is presently unknown, as specifically eliminating these cells is not possible, given that potentially targetable cell-surface markers are shared with other immune cells. Likewise, selectively and completely inhibiting ILC2 activation is also not currently possible, as several activating cytokines, IL-25, IL-33, and TSLP, act in redundancy or are not specific for ILC2 stimulation. Therefore, at this point, we can only identify the relative abundance of ILC2s in organs and tissue identified as being involved in specific diseases, and the contribution of ILC2s in human disease can only be inferred from mouse studies. Given these limitations, in this article, we will review the studies that have examined the presence of ILC2s in human disease states and speculate on their possible role in disease pathogenesis. The intent of the review is to identify priority areas for basic research based on clinical research insights.
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