Microbe-dependent lymphatic migration of neutrophils modulates lymphocyte proliferation in lymph nodes
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Neutrophil recruitment to the site of injury is an essential first step of an anti-bacterial response. However, little is known about the basis for and relevance of neutrophil migration from inflamed tissue into lymphoid organs. We established a photoconversion-based system to monitor the fate of neutrophils recruited to inflamed skin. While neutrophils are efficiently recruited to sites of both microbial and sterile lesions, subsequent re-localization to draining lymph nodes happens only when bacteria are present in the primary lesion. Skin egress of neutrophils occurs via lymphatic vessels and is dependent on CD11b and CXCR4 but not CCR7. Neutrophils are the predominant immune cell to migrate from inflamed skin into lymph nodes where they augment lymphocyte proliferation. Furthermore, inhibition of neutrophil migration from skin reduces T-cell proliferation in draining lymph nodes. Thus neutrophils mediate rapid cellular communication between the initial injury site and secondary lymphoid organs and modulate immune responsiveness.
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Entry of T cells and neutrophils into initial LVs is integrin-dependent under inflammatory conditions.
“Entry of T cells and neutrophils into initial LVs is also integrin-dependent under inflammatory conditions (112–114).”
From Transport and Immune Functions of the Lymphatic System. (2025) · cites this paper as [112]
The Results section ('CD11b and CXCR4 modulate neutrophil migration from skin'; page not available) reports that CD11b mediates neutrophil migration via lymphatic vessels from inflamed skin to draining lymph nodes. It does not establish integrin-dependent entry into initial lymphatic vessels specifically, or that T-cell entry is integrin-dependent. The observed lymphatic migration was also tied to microbial lesions, rather than inflammatory conditions generally. (LLM, conf=0.86)
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- Authors
- Hampton, H. R., Bailey, J., Tomura, M., Brink, R., & Chtanova, T.
- Affiliations
- Garvan Institute of Medical Research (AU)
- Osaka Ohtani University (JP)
- Corresponding author
- Chtanova, Tatyana
- Venue
- Nature Communications
- Published
- 2015-05-14
- Volume
- 6
- Issue
- 1
- Pages
- 7139-7139
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4479041
- OpenAlex
- W2222331351
- Cited by
- 211
- References
- 47
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 19 · 2023: 15 · 2022: 24 · 2021: 32 · 2020: 18 · 2019: 22 · 2018: 20 · 2017: 18 · 2016: 23 · 2015: 3
- FWCI
- 9.32
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Medical Research Council
- National Health and Medical Research Council (1062328, 1012858)
- Topics
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- neutrophil migration, lymphatic migration, draining lymph nodes, lymphocyte proliferation, skin inflammation, bacterial infection, sterile inflammation, CD11b, CXCR4, CCR7, T cell proliferation, secondary lymphoid organs
- MeSH terms
- Animals, Bacterial Infections, Cell Movement, Female, Immune System, Inflammation, Lymph Nodes, Lymphocyte Activation, Lymphocytes, Male, Mice, Inbred C57BL, Neutrophils, Phenotype, Skin, Staphylococcus aureus, Receptors, CXCR4, Neutrophil Infiltration, CD11b Antigen, Lymphatic Vessels, Mice, Receptors, CCR7
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