umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • 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
CNS: Not an immunoprivilaged site anymore but a virtual secondary lymphoid organ
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine).
2018 (English)In: International Reviews of Immunology, ISSN 0883-0185, E-ISSN 1563-5244, Vol. 37, no 1, p. 57-68Article, review/survey (Refereed) Published
Abstract [en]

The cardinal dogma of central nervous system (CNS) immunology believed brain is an immune privileged site, but scientific evidences gathered so far have overturned this notion proving that CNS is no longer an immune privileged site, but rather an actively regulated site of immune surveillance. Landmark discovery of lymphatic system surrounding the duramater of the brain, made possible by high resolution live imaging technology has given new dimension to neuro-immunology. Here, we discuss the immune privilege status of CNS in light of the previous and current findings, taking into account the differences between a healthy state and changes that occur during an inflammatory response. Cerebrospinal fluid (CSF) along with interstitial fluid (ISF) drain activated T cells, natural killer cells, macrophages and dendritic cells from brain to regional lymph nodes present in the head and neck region. To keep an eye on inflammation, this system hosts an army of regulatory T cells (CD25+ FoxP3+) that regulate T cell hyper activation, proliferation and cytokine production. This review is an attempt to fill the gaps in our understanding of neuroimmune interactions, role of innate and adaptive immune system in maintaining homeostasis, interplay of different immune cells, immune tolerance, knowledge of communication pathways between the CNS and the peripheral immune system and lastly how interruption of immune surveillance leads to neurodegenerative diseases. We envisage that discoveries should be made not only to decipher underlying cellular and molecular mechanisms of immune trafficking, but should aid in identifying targeted cell populations for therapeutic intervention in neurodegenerative and autoimmune disorders.

Place, publisher, year, edition, pages
Taylor & Francis, 2018. Vol. 37, no 1, p. 57-68
Keywords [en]
Astrocytes, blood-brain barrier, CNS, microglia, lymphatics
National Category
Immunology
Identifiers
URN: urn:nbn:se:umu:diva-144964DOI: 10.1080/08830185.2017.1357719ISI: 000424246300005PubMedID: 28961037OAI: oai:DiVA.org:umu-144964DiVA, id: diva2:1184583
Available from: 2018-02-21 Created: 2018-02-21 Last updated: 2018-06-09Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMed

Authority records BETA

Negi, Neema

Search in DiVA

By author/editor
Negi, Neema
By organisation
Department of Molecular Biology (Faculty of Medicine)
In the same journal
International Reviews of Immunology
Immunology

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 65 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • 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