Kuscher, Katrin; Danelon, Gabriela; Paoletti, Samantha; Stefano, Luisa; Schiraldi, Milena; Petkovic, Vibor; Locati, Massimo; Gerber, Basil O; Uguccioni, Mariagrazia (2009). Synergy-inducing chemokines enhance CCR2 ligand activities on monocytes. European journal of immunology, 39(4), pp. 1118-1128. Weinheim: Wiley-VCH 10.1002/eji.200838906
Full text not available from this repository. (Request a copy)The migration of monocytes to sites of inflammation is largely determined by their response to chemokines. Although the chemokine specificities and expression patterns of chemokine receptors are well defined, it is still a matter of debate how cells integrate the messages provided by different chemokines that are concomitantly produced in physiological or pathological situations in vivo. We present evidence for one regulatory mechanism of human monocyte trafficking. Monocytes can integrate stimuli provided by inflammatory chemokines in the presence of homeostatic chemokines. In particular, migration and cell responses could occur at much lower concentrations of the CCR2 agonists, in the presence of chemokines (CCL19 and CCL21) that per se do not act on monocytes. Binding studies on CCR2(+) cells showed that CCL19 and CCL21 do not compete with the CCR2 agonist CCL2. Furthermore, the presence of CCL19 or CCL21 could influence the degradation of CCL2 and CCL7 on cells expressing the decoy receptor D6. These findings disclose a new scenario to further comprehend the complexity of chemokine-based monocyte trafficking in a vast variety of human inflammatory disorders.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Paediatric Medicine |
UniBE Contributor: |
Petkovic, Vibor |
ISSN: |
0014-2980 |
ISBN: |
19291700 |
Publisher: |
Wiley-VCH |
Language: |
English |
Submitter: |
Anette van Dorland |
Date Deposited: |
04 Oct 2013 15:03 |
Last Modified: |
05 Dec 2022 14:19 |
Publisher DOI: |
10.1002/eji.200838906 |
PubMed ID: |
19291700 |
Web of Science ID: |
000265478700022 |
URI: |
https://boris.unibe.ch/id/eprint/27230 (FactScience: 105098) |
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