ILC1: Development, maturation, and transcriptional regulation

Abstract

Type 1 Innate Lymphoid cells (ILC1s) are tissue-resident cells that partake in the regulation of inflammation and homeostasis. A major feature of ILC1s is their ability to rapidly respond after infections. The effector repertoire of ILC1s includes the pro-inflammatory cytokines IFN-γ and TNF-α and cytotoxic mediators such as granzymes, which enable ILC1s to establish immune responses and to directly kill target cells. Recent advances in the characterization of ILC1s have considerably furthered our understanding of ILC1 development and maintenance in tissues. In particular, it has become clear how ILC1s operate independently from conventional natural killer cells, with which they share many characteristics. In this review, we discuss recent developments with regards to the differentiation, polarization, and effector maturation of ILC1s. These processes may underlie the observed heterogeneity in ILC1 populations within and between different tissues. Next, we highlight transcriptional programs that control each of the separate steps in the differentiation of ILC1s. These transcriptional programs are shared with other tissue-resident type-1 lymphocytes, such as tissue-resident memory T cells (T RM ) and invariant natural killer T cells (iNKT), highlighting that ILC1s utilize networks of transcriptional regulation that are conserved between lymphocyte lineages to respond effectively to tissue-invading pathogens.

Macrophage STING signaling promotes NK cell to suppress colorectal cancer liver metastasis via 4-1BBL/4-1BB co-stimulation

“… 39 40 However, recent discovery of functional characteristics and transcriptional programs shared by ILC1s and NK cells has made it difficult to distinguish them unequivocally. 41 In addition, conventional NK cells have been found to acquire ILC1 characteristics under certain conditions such as in a cancer setting, which may complicate the identification of NK cells and ILC1s. 42 43 In the present study, the potential role of ILC1s were not excluded and analyzed precisely.…”

Inflammation in HIV and Its Impact on Atherosclerotic Cardiovascular Disease

“…This activation fosters the formation of foam cells and exacerbates endothelial dysfunction, ultimately promoting plaque destabilization. 170 On the other hand, ILC3s, with their production of IL-17A and IL-22, further intensify the inflammatory environment within arterial walls. IL-17 promotes the recruitment of neutrophils and macrophages, while IL-22 exhibits both protective and pathogenic effects.…”

People are an organic unity: Gut-lung axis and pneumonia

“…ratified by the International Union of Immunological Societies (IUIS), ILCs were composed of five subgroups according to their growth and feature: Natural killer (NK) cells, ILC1, ILC2, ILC3, and lymphoid tissue-inducer (LTi) cells [ 17 ]. NK cells mainly exist in secondary lymphatic tissue, circulation, and some peripheral organs, while ILC1 is mainly distributed in the liver, salivary glands, small intestinal epithelial and lamina propria, uterus, and adipose tissue of the internal organs [ 18 ]. NK cells and ILC1 mainly produce interferon γ (IFN-γ), tumor necrosis factor α (TNF-α), and mediators of cytotoxicity, e.g., granzymes.…”