the activity of ccl18 is principally mediated through interaction with glycosaminoglycans

Clicks: 262
ID: 252101
2013
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Popular

Ranked #395 of 644 articles by views in sudebno-meditsinskaia ekspertiza

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 644 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
The CC chemokine ligand 18 (CCL18) was first identified as a chemoattractant for naïve T cells. It has been reported to recruit T and B lymphocytes, and we show here, Natural killer (NK) cells, but with low efficacy. Investigation of its ability to elicit G-protein coupled signaling showed that it does not involve extracellular signal-regulated kinase (ERK) phosphorylation, and it is not able to induce receptor internalization, as assessed on CCR3. CCL18 has recently been reported to possess activities unrelated to cellular recruitment, but it had no effect on T lymphocyte proliferation. We postulated that a more potent chemoattractant may be produced under inflammatory conditions but only minor truncations were observed, with the major form being the full-length protein. In view of the lack of potent immunomodulatory properties, we wondered if binding to CCL18 by the tick chemokine binding proteins (CkBPs) Evasin-1 and Evasin-4 was an artifact of the methods used, but complex formation was confirmed by size exclusion chromatography, and abrogation of its binding to, and antagonism of, CCR3. Its receptor has remained elusive since its cloning in 1997, although it has been reported to induce migration of breast cancer cells by signaling through PITPNM3, but we show that this receptor is not expressed on lymphocytes. We have developed a radiolabelled equilibrium competition binding assay and demonstrated that it bound with high affinity to peripheral blood leukocytes (PBLs), but the binding was displaced similarly by both unlabelled CCL18 as well as heparin. Both heparin binding and binding to PBLs are considerably abrogated by mutation of the BBXB motif in the 40s loop suggesting an essential role of the CCL18-glycosaminoglycan (GAG) interaction.
Reference Key
krohn2013frontiersthe Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Sonja C. Krohn;Alexandre eGarin;Cem eGabay;Amanda E.I. Proudfoot
Journal sudebno-meditsinskaia ekspertiza
Year 2013
DOI
10.3389/fimmu.2013.00193
URL
http://journal.frontiersin.org/Journal/10.3389/fimmu.2013.00193/full
Keywords
chemokines synovial fluid ccl18 allergy

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.