BioAcyl Corp
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Pradeu, T., Thomma, B. P. H. J., Girardin, S. E., & Lemaitre, B. (2024). The conceptual foundations of innate immunity: Taking stock 30 years later. Immunity, 54(4), 613–631. Added by: Dr. Enrique Feoli (26/12/2025, 17:32) Last edited by: Dr. Enrique Feoli (26/12/2025, 17:46) |
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| Resource type: Journal Article ID no. (ISBN etc.): 1074-7613 BibTeX citation key: Pradeu2024 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Innate Immunity Creators: Girardin, Lemaitre, Pradeu, Thomma Collection: Immunity |
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| Abstract |
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While largely neglected over decades during which adaptive immunity captured most of the attention, innate immune mechanisms have now become central to our understanding of immunology. Innate immunity provides the first barrier to infection in vertebrates, and it is the sole mechanism of host defense in invertebrates and plants. Innate immunity also plays a critical role in maintaining homeostasis, shaping the microbiota, and in disease contexts such as cancer, neurodegeneration, metabolic syndromes, and aging. The emergence of the field of innate immunity has led to an expanded view of the immune system, which is no longer restricted to vertebrates and instead concerns all metazoans, plants, and even prokaryotes. The study of innate immunity has given rise to new concepts and language. Here, we review the history and definition of the core concepts of innate immunity, discussing their value and fruitfulness in the long run.
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |
| Notes |
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(A) PAMPs-triggered immunity (PTI). Structural molecules specific to a class of microbes (PAMPs/MAMPs) are recognized by host pattern recognition receptors (PRRs), which trigger the immune response. PRRs can bind directly to microbes (e.g., PGRP-SA to Gram-positive bacteria) or more frequently sense microbes by sensing MAMPs released by microbes (indirect mode). PRRs can be secreted, transmembrane, phagosomal, or intracellular (not shown). They can initiate a transcriptional program or directly trigger effector modules.
(B) Effector-triggered immunity (ETI). Host receptors directly sense virulence factors, or more frequently “guard proteins” sense the activity of virulence factors that modify host molecules. There are multiple variations on the mechanisms that allow the sensing of microbial effectors (not shown here, e.g., decoys20). Host guard proteins can be extracellular (e.g., detection of microbial protease activity in Drosophila by Persephone), transmembrane, or intracellular.
(C) Recognition of the absence of self. The immune system is activated when a constitutive signal provided by host cells is not detected by host receptors, indicating material of foreign origin.
(D) Recognition of altered self. Some immune receptors can recognize altered or abnormal self-patterns. This is often a host component located at a place where it is normally absent, such as a normally intracellular molecule present in extracellular spaces.
(E) Recognition of damage-associated molecular patterns (DAMPs). Innate immune responses are triggered by the sensing of host molecules released upon damage to host tissues.
(F) Surveillance. Innate immune responses are triggered by generalist stress pathways that interpret rupture of cellular homeostasis as an indicator of infection.
Sensing mechanisms are either direct (pink background) or indirect via the sensing of activities or damages (green background).
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |
