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Control of adaptive immunity by the innate immune system
Open accessAbstract
Microbial infections are recognized by the innate immune system both to elicit immediate defense and to generate long-lasting adaptive immunity. To detect and respond to vastly different groups of pathogens, the innate immune system uses several recognition systems that rely on sensing common structural and functional features associated with different classes of microorganisms. These recognition systems determine microbial location, viability, replication and pathogenicity. Detection of these features by recognition pathways of the innate immune system is translated into different classes of effector responses though specialized populations of dendritic cells. Multiple mechanisms for the induction of immune responses are variations on a common design principle wherein the cells that sense infections produce one set of cytokines to induce lymphocytes to produce another set of cytokines, which in turn activate effector responses. Here we discuss these emerging principles of innate control of adaptive immunity.
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“TLRs do not directly initiate phagocytosis but facilitate it more effectively [27].”
From Insights of Endocytosis Signaling in Health and Disease (2023) · cites this paper as [27]
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“In more than 400 healthy, middle to early old age participants drawn from the Whitehall II Cohort study, self-reported short sleep duration in men, but not in women, was related to shorter leukocyte telomere length”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [267]
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“Live attenuated vaccines induce immunity by stimulating the innate immune system and providing antigen to specify the adaptive immune responses (Iwasaki and Medzhitov, 2015).”
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Metadata
- Authors
- Iwasaki, A., & Medzhitov, R.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Iwasaki, Akiko
- Medzhitov, Ruslan
- Venue
- Nature Immunology
- Published
- 2015-03-19
- Volume
- 16
- Issue
- 4
- Pages
- 343-353
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC4507498
- OpenAlex
- W2044757050
- Cited by
- 2,160
- References
- 139
- Citations by year
- 2026: 183 · 2025: 212 · 2024: 181 · 2023: 193 · 2022: 204 · 2021: 239 · 2020: 216 · 2019: 189 · 2018: 187 · 2017: 167 · 2016: 157 · 2015: 31
- FWCI
- 17.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute of Allergy and Infectious Diseases (R01AI064705, AI062428, AI 064705, R01AI062428, AI 081884, R56AI062428, AI089771, R01AI089771, R01AI054359, R37AI046688, AI046688, R01AI081884, R01AI046688)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK071754, R01DK071754)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- innate immunity, adaptive immunity, innate-adaptive immune crosstalk, pathogen recognition, dendritic cells, cytokines, lymphocyte activation, microbial infection, pattern recognition receptors
- MeSH terms
- Animals, Bacteria, Dendritic Cells, Fungi, Gene Expression Regulation, Helminths, Humans, Immunity, Innate, Intestines, Lung, Skin, Viruses, Lymphocyte Subsets, Cytokines, Receptors, Pattern Recognition, Adaptive Immunity
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