Résumé
Innate lymphoid cells (ILCs) are the most recently discovered family of innate immune cells, derived from common lymphoid progenitors (CLPs). 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 (immune associated), and non- lymphoid tissues, and rarely in the 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 regular lymphoid morphology, absence of rearranged antigen receptors found on T cells and B cells (due to the lack of the RAG gene), 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, they are now divided into five groups: NK cells, ILC1s, ILC2s, ILC3s, and lymphoid tissue inducer (LTi) cells. ILCs are implicated in multiple physiological functions, including tissue homeostasis, morphogenesis, metabolism, repair, and regeneration. Many of their roles are similar to T cells, therefore they have been suggested to be the innate counterparts of T cells. The dysregulation of ILCs can lead to immune pathology such as allergy, bronchial asthma and autoimmune disease. The development of ILCs is initiated in response to the presence of transcription factors that are switched on due to the presence of surrounding microenvironmental factors, such as: cytokines, notch ligands, and circadian rhythm (inbuilt behavioural changes following a daily cycle). Once matured, the ILCs release cytokines. The classification of ILCs is therefore based on the differences in the transcription factor and cytokine profiles associated with the development and function of the different ILC subtypes.
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