Abstract
Since their identification as a unique cell population, innate lymphoid cells (ILCs) have revolutionized our understanding of immune responses, leaving their impact on multiple inflammatory and fibrotic pathologies without doubt. Thus, a tightly controlled regulation of local ILC numbers and their activity is of crucial importance. Even though this has been extensively studied in murine ILCs in the last few years, our knowledge of human ILCs is still lagging behind. Our review article will therefore summarize recent insights into the function of human ILCs and will particularly focus on their regulation under inflammatory conditions. The quality and intensity of ILC involvement into local immune responses at mucosal sites of the human body can potentially be modulated via three different axes: (1) activation of tissue-resident mature ILCs, (2) plasticity and local transdifferentiation of specific ILC subsets, and (3) tissue migration and accumulation of peripheral ILCs. Despite a still ongoing scientific effort in this field, already existing data on the fate of human ILCs under different pathologic conditions clearly indicate that all three of these mechanisms are of relevance for the clinical course of chronic inflammatory and autoimmune diseases and might likewise provide new target structures for future therapeutic strategies.
Highlights
Having been overlooked for ages, helper innate lymphoid cells (ILCs) have been increasingly recognized as key immunological players since their discovery as a distinct cell population in 2010 [1,2,3]
In the case of human ILC1s, the pro-inflammatory cytokine IL-12, which has already been well-known for its ability to promote type-1 immune responses [121], turned out to be of immense importance for the activation of ILC1s and subsequent IFN-γ release [15, 78] as shown in primary human ILC1s purified from tonsils and peripheral blood [15, 78]
Upon stimulation by IL-33, which is rapidly released by epithelial cells sensing stress signals in vivo [166], ICAM-1 expression was upregulated in human ILC2s [93], indicating the importance of this interaction for mounting efficient ILC2 responses
Summary
Having been overlooked for ages, helper innate lymphoid cells (ILCs) have been increasingly recognized as key immunological players since their discovery as a distinct cell population in 2010 [1,2,3]. In the case of human ILC1s, the pro-inflammatory cytokine IL-12, which has already been well-known for its ability to promote type-1 immune responses [121], turned out to be of immense importance for the activation of ILC1s and subsequent IFN-γ release [15, 78] as shown in primary human ILC1s purified from tonsils and peripheral blood [15, 78].
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