page_title: Innate lymphoid cell
section_title: Inflammatory bowel disease (IBD), and intestinal cancer
hierarchical_section_title: Innate lymphoid cell / Pathology / Inflammatory bowel disease (IBD), and intestinal cancer
caption_attribution_description: English: ILCs involved in the pathophysiology of IBD.
context_page_description: Innate lymphoid cells are the most recently discovered family of innate immune cells, derived from common lymphoid progenitors. In response to pathogenic tissue damage, ILCs contribute to immunity via the secretion of signalling molecules, and the regulation of both innate and adaptive immune cells. ILCs are primarily tissue resident cells, found in both lymphoid, and non- lymphoid tissues, and rarely in the peripheral blood. They are particularly abundant at mucosal surfaces, playing a key role in mucosal immunity and homeostasis. Characteristics allowing their differentiation from other immune cells include the absence of regular lymphoid morphology, rearranged antigen receptors found on T cells and B cells, and phenotypic markers usually present on myeloid or dendritic cells.
  Based on the difference in developmental pathways, phenotype, and signalling molecules produced, in 2013, ILCs were divided into three groups: 1, 2 and 3, however, after further investigation, we now appreciate five distinct subsets within these groups: NK cells, ILC1s, ILC2s, ILC3s, and LTi cells.
context_section_description: Research suggests IL-17 producing NCR- ILC3s contribute to the pathophysiology of IBD due to their increased abundance in the intestine of patients with Crohn’s disease. In addition, the number of ILC1s in the intestinal mucosa of patients with Crohn’s disease is increased from approximately 10% to 40% of the total ILCs present. The increase in ILCs present correlates with the severity of the disease. Evidence suggests that the plasticity between ILC3s and ILC1s in the intestine is an important factor of Crohn’s disease, with ILC3s differentiating into ILC1s when exposed to IL-12 produced by dendritic cells. However, IL-23, IL-1B and retinoic acid present in the intestine can drive the differentiation of ILC1s back to ILC3s. Evidence also suggests the ability of ILC2s to acquire the pro-inflammatory phenotype, with ILC2s producing IFN-γ present in the intestine of patients with Crohn’s disease, in response to certain environmental factors such as cytokines. 
  Patients with IBD have an increased risk of getting intestinal cancer due to chronic inflammation, when the ILC3s acquire the ILC1 pro-inflammatory phenotype during chronic inflammation. Since ILCs accumulate in the intestine of IBD patients, it is believed they may have a pro-tumorigenic role. Supporting this, studies show an increase in the amount of effector cytokines IL-23, IL-17, and IL-22, in the tumor microenvironment of intestinal cancer.
  NK cells secrete IFN-γ, which has anti-tumorigenic effects. Multiple studies show a decreased frequency of NK cells and IFN-γ present in the intestine or peripheral blood of patients with intestinal cancer. Further studies are required to address their exact role in the intestinal cancer environment.
caption: The ILCs present in the intestine of patients with IBD, and the effector cytokines and cells contributing to the pathophysiology of the disease.[38]
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