uu.seUppsala universitets publikationer
Ändra sökning
RefereraExporteraLänk till posten
Permanent länk

Direktlänk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Early Detection of Peripheral Blood Cell Signature in Children Developing beta-Cell Autoimmunity at a Young Age
Univ Turku, Turku Biosci Ctr, Turku, Finland; Åbo Akad Univ, Turku, Finland.
Aalto Univ, Dept Comp Sci, Sch Sci, Espoo, Finland.
Univ Turku, Turku Biosci Ctr, Turku, Finland; Åbo Akad Univ, Turku, Finland.
Univ Turku, Turku Biosci Ctr, Turku, Finland; Åbo Akad Univ, Turku, Finland.
Visa övriga samt affilieringar
2019 (Engelska)Ingår i: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 68, nr 10, s. 2024-2034Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The appearance of type 1 diabetes (T1D)-associated autoantibodies is the first and only measurable parameter to predict progression toward T1D in genetically susceptible individuals. However, autoantibodies indicate an active autoimmune reaction, wherein the immune tolerance is already broken. Therefore, there is a clear and urgent need for new biomarkers that predict the onset of the autoimmune reaction preceding autoantibody positivity or reflect progressive beta-cell destruction. Here we report the mRNA sequencing-based analysis of 306 samples including fractionated samples of CD4(+) and CD8(+) T cells as well as CD4(-)CD8(-) cell fractions and unfractionated peripheral blood mononuclear cell samples longitudinally collected from seven children who developed beta-cell autoimmunity (case subjects) at a young age and matched control subjects. We identified transcripts, including interleukin 32 (IL32), that were upregulated before T1D-associated autoantibodies appeared. Single-cell RNA sequencing studies revealed that high IL32 in case samples was contributed mainly by activated T cells and NK cells. Further, we showed that IL32 expression can be induced by a virus and cytokines in pancreatic islets and beta-cells, respectively. The results provide a basis for early detection of aberrations in the immune system function before T1D and suggest a potential role for IL32 in the pathogenesis of T1D.

Ort, förlag, år, upplaga, sidor
2019. Vol. 68, nr 10, s. 2024-2034
Nationell ämneskategori
Endokrinologi och diabetes
Identifikatorer
URN: urn:nbn:se:uu:diva-395419DOI: 10.2337/db19-0287ISI: 000487068200014PubMedID: 31311800OAI: oai:DiVA.org:uu-395419DiVA, id: diva2:1363022
Forskningsfinansiär
EU, Horisont 2020Novo Nordisk, 115797EU, FP7, Sjunde ramprogrammet, 202063Tillgänglig från: 2019-10-22 Skapad: 2019-10-22 Senast uppdaterad: 2019-10-22Bibliografiskt granskad

Open Access i DiVA

Fulltext saknas i DiVA

Övriga länkar

Förlagets fulltextPubMed

Personposter BETA

Anagandula, Mahesh KumarFrisk, Gun

Sök vidare i DiVA

Av författaren/redaktören
Anagandula, Mahesh KumarFrisk, GunLund, Riikka
Av organisationen
Klinisk immunologi
I samma tidskrift
Diabetes
Endokrinologi och diabetes

Sök vidare utanför DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetricpoäng

doi
pubmed
urn-nbn
Totalt: 2 träffar
RefereraExporteraLänk till posten
Permanent länk

Direktlänk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf