Sepsis is a life-threatening syndrome caused by a dysregulated host response to infection, resulting in very high mortality. Dysfunction of the tightly regulated immune response occurs when the body exerts an exacerbated hyperinflammatory response that is counteracted by an anti-inflammatory response, which results in immune paralysis if it is sustained for long.
Innate lymphoid cells (ILCs) are immune effector cells of lymphoid origin that are devoid of recombination-activating gene-dependent rearranged antigen receptors, as in T and B cells.1 This evolutionary adaptation eliminates the necessity for antigen presentation to activate these cells, and therefore, these cells can rapidly sense and respond to infection and inflammation. ILCs sense tissue injury and pathogen infiltration through numerous cytokine, chemokine, and pattern recognition receptors. ILCs are of lymphoid origin and arise from a common lymphoid progenitor (CLP). Since ILCs share several common features with T cells, the evolutionary model suggests that ILCs are the primordial T-cell precursor. The requirement for the transcriptional repressor ID2 in the development of ILCs suggests that these cells might have originated from a common ID2-dependent progenitor. Recently, ILCs have been categorized into Group 1, Group 2, and Group 3 ILCs with different subsets in each group (Fig. 1).1 A subpopulation of ILCs called ILC regulatory cells (ILCregs) has been identified, and these cells are functionally similar to T regulatory cells (Tregs).2
Theertha M., S., S., Priya, V. V., Jain, P., Dr. Praveen Varma, and Dr. Ullas Mony, “Innate Lymphoid Cells: Potent Early Mediators of the Host Immune Response During Sepsis”, Cellular and Molecular Immunology, 2020.