Innate Immunity
Summary
Innate immunity constitutes the body’s first line of defence against infection and tissue disruption. It relies on physical barriers such as skin and mucosa, cellular sentinels including neutrophils, macrophages, dendritic cells and innate lymphoid cells, and soluble mediators such as complement proteins, antimicrobial peptides and pro-inflammatory cytokines. Germline-encoded pattern recognition receptors—toll-like receptors, C-type lectins, NOD-like receptors, RIG-I-like receptors and the cGAS–STING axis—detect conserved microbial motifs or danger signals, triggering phagocytosis, inflammatory cascades and cell-death programmes like pyroptosis. Complement activation amplifies opsonisation, cell lysis and leukocyte recruitment. Resolution is driven by specialised pro-resolving lipid mediators and efferocytosis to restore tissue homeostasis. The speed and breadth of innate responses underpin vaccine efficacy, antimicrobial therapies and interventions in chronic inflammation and immunometabolic disease.
Research from Nature Portfolio
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Research from all publishers
Atomic-level structures of the complement fragment C5a bound to its G-protein-coupled receptor C5aR1 have clarified how force-dependent catch and slip bonds direct biased signalling via G proteins or β-arrestins. By altering bond lifetimes under shear, the receptor averts premature neutrophil priming in vivo and maintains vascular homeostasis, offering a template for designing selective C5aR1 modulators that temper inflammation without compromising host defence.
A comprehensive review of inflammasomes has expanded the canonical repertoire of intracellular sensors to include novel receptors such as NLRP6, NLRP9 and CARD8. Distinct ligands—from bacterial cell-wall fragments to viral RNAs—trigger specific oligomerisation pathways and tissue-restricted inflammatory outcomes. Early translational efforts with selective inhibitors of these emerging inflammasomes show promise in colitis, neuroinflammation and metabolic dysfunction.
Studies on immunometabolism have revealed bidirectional interactions between innate sensors and cellular energy pathways. Activation of NLRs can reprogramme mitochondrial function and reactive oxygen species generation to modulate inflammatory outputs, while shifts in glycolytic and oxidative flux set activation thresholds for inflammasome assembly and type I interferon responses. This metabolic-immune interface offers new strategies to fine-tune innate responses in infection and chronic inflammatory conditions.
Innate Immunity publication trend
The graph below shows the total number of articles in innate immunity across all publications each year (not limited to Nature Index journals).
Technical terms
Pattern recognition receptor: A germline-encoded sensor that binds conserved microbial or danger motifs to initiate innate responses.
Inflammasome: A multiprotein complex, often formed by NLRP3 or NLRC4, that recruits and activates caspase-1 to process IL-1β and induce pyroptosis.
Pyroptosis: A lytic, gasdermin-driven form of inflammatory programmed cell death.
Anaphylatoxin: Complement fragments (C3a, C5a) that promote inflammation by recruiting and activating leukocytes.
Complement convertase: An enzyme complex (C4b2a or C3bBb) responsible for proteolytic cleavage and amplification of complement proteins.
Catch/slip bond: A receptor–ligand interaction whose lifetime increases (catch) or decreases (slip) under mechanical force.
Specialised pro-resolving mediator: An endogenous lipid derived from essential fatty acids that actively orchestrates the termination of inflammation.
References
- Mechanism of activation and biased signaling in complement receptor C5aR1. Cell Research (2023).
- Molecular mechanisms of emerging inflammasome complexes and their activation and signaling in inflammation and pyroptosis. Immunological Reviews (2024).
- Impact of intracellular innate immune receptors on immunometabolism. Cellular & Molecular Immunology (2021).
- Innate Immunity: Recognition and Effector Functions.
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