Innate lymphoid cells: critical regulators of allergic inflammation and tissue repair in the lung

Abstract

Maintenance of epithelial barrier function in the skin, respiratory tract and intestine is critical to limit exposure to commensal and pathogenic microbes and to maintain tissue homeostasis. Innate lymphoid cells (ILCs) are a recently recognized innate immune cell population that plays critical roles in host defense, regulation of inflammation and promotion of wound healing and tissue repair at barrier surfaces. In this review we discuss recent advances in the understanding of how ILC populations in the respiratory tract impact allergic airway inflammation and lung epithelial repair.

Figure 1. Regulation, phenotype and function of lung-resident Type 2 ILCs

In the lung, numerous infectious and allergic stimuli can promote epithelial cell and macrophage expression of IL-33. IL-33, IL-2 and IL-7 have been shown to act on Type 2 ILCs (defined as Lin⁻ cells that express ST2, CD127, CD25 and c-Kit) to induce expression of autocrine IL-9 and paracrine IL-5, IL-13 and amphiregulin (Areg) that, depending on the context, can induce either pathologic allergic airway inflammation or protective airway tissue repair.