Endogenous and recombinant type I interferons and disease activity in multiple sclerosis.

Although treatment of multiple sclerosis (MS) with the type I interferon (IFN) IFN-β lowers disease activity, the role of endogenous type I IFN in MS remains controversial. We studied CD4+ T cells and CD4+ T cell subsets, monocytes and dendritic cells by flow cytometry and analysed the relationship...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Finn Sellebjerg, Martin Krakauer, Signe Limborg, Dan Hesse, Henrik Lund, Annika Langkilde, Helle Bach Søndergaard, Per Soelberg Sørensen
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2012
Materias:
R
Q
Acceso en línea:https://doaj.org/article/6a9834ea9d174e548aeecffd4c7d52f9
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:6a9834ea9d174e548aeecffd4c7d52f9
record_format dspace
spelling oai:doaj.org-article:6a9834ea9d174e548aeecffd4c7d52f92021-11-18T07:16:16ZEndogenous and recombinant type I interferons and disease activity in multiple sclerosis.1932-620310.1371/journal.pone.0035927https://doaj.org/article/6a9834ea9d174e548aeecffd4c7d52f92012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22701554/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Although treatment of multiple sclerosis (MS) with the type I interferon (IFN) IFN-β lowers disease activity, the role of endogenous type I IFN in MS remains controversial. We studied CD4+ T cells and CD4+ T cell subsets, monocytes and dendritic cells by flow cytometry and analysed the relationship with endogenous type I IFN-like activity, the effect of IFN-β therapy, and clinical and magnetic resonance imaging (MRI) disease activity in MS patients. Endogenous type I IFN activity was associated with decreased expression of the integrin subunit CD49d (VLA-4) on CD4+CD26(high) T cells (Th1 helper cells), and this effect was associated with less MRI disease activity. IFN-β therapy reduced CD49d expression on CD4+CD26(high) T cells, and the percentage of CD4+CD26(high) T cells that were CD49d(high) correlated with clinical and MRI disease activity in patients treated with IFN-β. Treatment with IFN-β also increased the percentage of CD4+ T cells expressing CD71 and HLA-DR (activated T cells), and this was associated with an increased risk of clinical disease activity. In contrast, induction of CD71 and HLA-DR was not observed in untreated MS patients with evidence of endogenous type IFN I activity. In conclusion, the effects of IFN-β treatment and endogenous type I IFN activity on VLA-4 expression are similar and associated with control of disease activity. However, immune-activating effects of treatment with IFN-β may counteract the beneficial effects of treatment and cause an insufficient response to therapy.Finn SellebjergMartin KrakauerSigne LimborgDan HesseHenrik LundAnnika LangkildeHelle Bach SøndergaardPer Soelberg SørensenPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 6, p e35927 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Finn Sellebjerg
Martin Krakauer
Signe Limborg
Dan Hesse
Henrik Lund
Annika Langkilde
Helle Bach Søndergaard
Per Soelberg Sørensen
Endogenous and recombinant type I interferons and disease activity in multiple sclerosis.
description Although treatment of multiple sclerosis (MS) with the type I interferon (IFN) IFN-β lowers disease activity, the role of endogenous type I IFN in MS remains controversial. We studied CD4+ T cells and CD4+ T cell subsets, monocytes and dendritic cells by flow cytometry and analysed the relationship with endogenous type I IFN-like activity, the effect of IFN-β therapy, and clinical and magnetic resonance imaging (MRI) disease activity in MS patients. Endogenous type I IFN activity was associated with decreased expression of the integrin subunit CD49d (VLA-4) on CD4+CD26(high) T cells (Th1 helper cells), and this effect was associated with less MRI disease activity. IFN-β therapy reduced CD49d expression on CD4+CD26(high) T cells, and the percentage of CD4+CD26(high) T cells that were CD49d(high) correlated with clinical and MRI disease activity in patients treated with IFN-β. Treatment with IFN-β also increased the percentage of CD4+ T cells expressing CD71 and HLA-DR (activated T cells), and this was associated with an increased risk of clinical disease activity. In contrast, induction of CD71 and HLA-DR was not observed in untreated MS patients with evidence of endogenous type IFN I activity. In conclusion, the effects of IFN-β treatment and endogenous type I IFN activity on VLA-4 expression are similar and associated with control of disease activity. However, immune-activating effects of treatment with IFN-β may counteract the beneficial effects of treatment and cause an insufficient response to therapy.
format article
author Finn Sellebjerg
Martin Krakauer
Signe Limborg
Dan Hesse
Henrik Lund
Annika Langkilde
Helle Bach Søndergaard
Per Soelberg Sørensen
author_facet Finn Sellebjerg
Martin Krakauer
Signe Limborg
Dan Hesse
Henrik Lund
Annika Langkilde
Helle Bach Søndergaard
Per Soelberg Sørensen
author_sort Finn Sellebjerg
title Endogenous and recombinant type I interferons and disease activity in multiple sclerosis.
title_short Endogenous and recombinant type I interferons and disease activity in multiple sclerosis.
title_full Endogenous and recombinant type I interferons and disease activity in multiple sclerosis.
title_fullStr Endogenous and recombinant type I interferons and disease activity in multiple sclerosis.
title_full_unstemmed Endogenous and recombinant type I interferons and disease activity in multiple sclerosis.
title_sort endogenous and recombinant type i interferons and disease activity in multiple sclerosis.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/6a9834ea9d174e548aeecffd4c7d52f9
work_keys_str_mv AT finnsellebjerg endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
AT martinkrakauer endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
AT signelimborg endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
AT danhesse endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
AT henriklund endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
AT annikalangkilde endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
AT hellebachsøndergaard endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
AT persoelbergsørensen endogenousandrecombinanttypeiinterferonsanddiseaseactivityinmultiplesclerosis
_version_ 1718423669484552192