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Updated: Jun 19, 2026

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Published on: February 16, 2020
CD47 and TLR-2 cross-talk regulates neutrophil transmigration
Alex C Chin1, Bénédicte Fournier, Eric J Peatman
1Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA. achin@emory.edu
Toll-like receptor 2 (TLR2) and CD47 costimulation enhance neutrophil transmigration during acute inflammation. This interaction boosts the sensitivity of neutrophils to TLR2 activation, aiding their movement to infection sites for pathogen removal.
Area of Science:
- Immunology
- Cell Biology
Background:
- Neutrophil (PMN) infiltration is key to acute inflammation and pathogen clearance.
- CD47 regulates PMN transmigration, but its role with Toll-like receptor (TLR) signaling during microbial invasion is unclear.
Purpose of the Study:
- To investigate the combined roles of TLR2 and CD47 in regulating PMN transmigration.
- To understand how TLR2 and CD47 costimulation impacts neutrophil migration during microbial invasion.
Main Methods:
- Assessed human PMN transmigration across collagen-coated filters using TLR2 agonists (MALP-2, Pam(3)CSK(4)) and anti-CD47 antibodies.
- Utilized TLR2(-/-) and MyD88(-/-) deficient murine bone marrow-derived PMNs.
- Investigated the effect of MyD88 homodimerization inhibition on PMN transmigration.
Main Results:
- MALP-2 (TLR2/6 agonist) more significantly inhibited PMN transmigration than Pam(3)CSK(4) (TLR2/1 agonist).
- MALP-2 or anti-CD47 treatment delayed PMN migration; combined treatment caused further delay.
- MALP-2 increased surface CD11b expression on PMNs, but not CD47.
- TLR2 or MyD88 deficiency, or MyD88 homodimerization inhibition, reversed the effects of MALP-2 or anti-CD47 on PMN transmigration.
- CD47(-/-) PMNs showed reduced sensitivity to MALP-2.
Conclusions:
- CD47 signaling activation enhances PMN sensitivity to TLR2 activation.
- This costimulation facilitates neutrophil arrival at invasion sites, potentially enhancing antimicrobial functions.
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