uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Interacting Chemokine Signals Regulate Dendritic Cells in Acute Brain Injury
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Neuroscience.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Neuroscience.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Neuroscience.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
Show others and affiliations
2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 8, e104754- p.Article in journal (Refereed) Published
Abstract [en]

Brain trauma is known to activate inflammatory cells via various chemokine signals although their interactions remain to be characterized. Mice deficient in Ccl3, Ccr2 or Cxcl10 were compared with wildtype mice after controlled cortical impact injury. Expression of Ccl3 in wildtypes was rapidly upregulated in resident, regularly spaced reactive microglia. Ccl3-deficiency enhanced endothelial expression of platelet selectin and invasion of peripheral inflammatory cells. Appearance of Ccr2 transcripts, encoding the Ccl2 receptor, reflected invasion of lysozyme 2-expressing phagocytes and classical antigen-presenting dendritic cells expressing major histocompatibility complex class II. Ccr2 also directed clustered plasmacytoid dendritic cells positive for the T-cell attracting chemokine Cxcl10. A reduction in Ccr2 and dendritic cells was found in injured wildtype cortex after cyclophosphamide treatment resembling effects of Ccr2-deficiency. The findings demonstrate the feasibility to control inflammation in the injured brain by regulating chemokine-dependent pathways.

Place, publisher, year, edition, pages
2014. Vol. 9, no 8, e104754- p.
National Category
Neurology
Identifiers
URN: urn:nbn:se:uu:diva-233017DOI: 10.1371/journal.pone.0104754ISI: 000340952200024OAI: oai:DiVA.org:uu-233017DiVA: diva2:753570
Available from: 2014-10-08 Created: 2014-09-29 Last updated: 2017-12-05Bibliographically approved

Open Access in DiVA

fulltext(1061 kB)226 downloads
File information
File name FULLTEXT01.pdfFile size 1061 kBChecksum SHA-512
7b2c43a0719eae08c3f6363a45c4938ba691b04b0313db7703bb52e04699a3b13ca0724b1d3f20f44ec109f39495209de64bafde719cdb6376e927d93ad20b58
Type fulltextMimetype application/pdf

Other links

Publisher's full text

Authority records BETA

Israelsson, CharlotteKylberg, AnnikaHillered, LarsEbendal, Ted

Search in DiVA

By author/editor
Israelsson, CharlotteKylberg, AnnikaHillered, LarsEbendal, Ted
By organisation
Developmental NeuroscienceNeurosurgery
In the same journal
PLoS ONE
Neurology

Search outside of DiVA

GoogleGoogle Scholar
Total: 226 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

doi
urn-nbn

Altmetric score

doi
urn-nbn
Total: 691 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf