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Innate immunity corresponds to the non-specific response of the organism to pathogens and is mediated by mast cells, phagocytes (macrophages, neutrophils and dendritic cells), basophils, eosinophils, NK cells as well as γδ T cells. This first line of defence is found in all class of plants and animals (vertebrate or not). It is based on the recognition of Pathogen-Associated Molecular Patterns (PAMPs) or endogenous danger signals through the sensing of Danger-Associated Molecular Patterns (DAMPs) by pattern recognition receptors 1 (PRRs). Activation of PRRs triggers cell signalling leading to the production of proinflammatory cytokines, chemokines and type 1 interferons, the induction of antimicrobial and inflammatory responses, pyroptotic cell death and the recruitment of phagocytic cells. These innate responses are responsible for efficient destruction and clearance of invading pathogens and other molecular threats and instructing the development of an appropriate pathogen-specific adaptive immune response.

Innate immune system comprises several classes of PRRs that allow the early detection of pathogens at the site of infection. The membrane-bound Toll-like receptors (TLRs) and C-type lectin receptors2 (CLRs) detect PAMPs in extracellular and endosomal compartments. TLRs and CLRs cooperate with PRRs sensing the presence of cytosolic nucleic acids like RIG-I like helicases/receptor (RLH/RLR). Another set of intracellular sensing PRRs are NOD-like receptors (NLRs) able to recognise PAMPs and DAMPs.

Upon stress (including infection and metabolic deregulation), certain NLRs form high molecular weight complexes called inflammasomes. These complexes associated with autophagy play a central role in controlling innate and adaptive immunity.

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References:

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