Cited by 811Immune Response and InflammationCytokine Signaling Pathways and InteractionsInflammation biomarkers and pathways

IL-6: a regulator of the transition from neutrophil to monocyte recruitment during inflammation

Kaplanski, G·2003·Trends in Immunology

Abstract

The origin of the Toll-like family of receptors pre-dates the evolutionary split between the plant and animal kingdoms. These receptors are remarkably conserved across the taxonomic kingdoms and have fundamental roles in triggering immune responses. How they trigger such responses, and how these mechanisms arose in evolution, is a topic of extensive debate. We postulate a surveillance model: these receptors "keep watch" for both endogenous and exogenous molecules that indicate tissue inquiry, infection and remodeling. Furthermore, we suggest that the first Toll-like family receptors that arose in evolution might have acted in both development and immunity by recognizing the degradation of endogenous macromolecules.

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Crossref · 10.1016/s1471-4906(02)00013-3

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Authors
Kaplanski, G.
Affiliations
Inserm (FR)
Corresponding author
Kaplanski, G
Venue
Trends in Immunology
Publisher
Elsevier BV
Published
2003-01
Volume
24
Issue
1
Pages
25-29
ISSN
1471-4906 (ISSN-L)
OpenAlex
W2091169302
Cited by
811
References
39
Citations by year
2026: 24 · 2025: 29 · 2024: 27 · 2023: 29 · 2022: 39 · 2021: 56 · 2020: 62 · 2019: 33 · 2018: 37 · 2017: 49 · 2016: 53 · 2015: 29 · 2014: 31 · 2013: 39 · 2012: 36
FWCI
7.33
Type
journal article
Language
en
Open access
closed
Locations
  • Trends in Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
interleukin-6, neutrophil recruitment, monocyte recruitment, inflammation, Toll-like receptors, immune system evolution, innate immunity
MeSH terms
Animals, Cell Movement, Humans, Inflammation, Lymph Nodes, Models, Biological, Monocytes, Neutrophils, Signal Transduction, Interleukin-6, Apoptosis, Receptors, Interleukin-6, Mice

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