WFRF:(Magnusson Mattias)
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 04772naa a2200313 4500 | |
| 001 | oai:DiVA.org:liu-102367 | |
| 003 | SwePub | |
| 008 | 131209s2013 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1023672 URI |
| 024 | 7 | a https://doi.org/10.1186/ar43262 DOI |
| 040 | a (SwePub)liu | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Chalise, Jaya Prakashu Linköpings universitet,Avdelningen för inflammationsmedicin,Hälsouniversitetet4 aut0 (Swepub:liu)jaypr20 |
| 245 | 1 0 | a Interferon alpha inhibits antigen-specific production of proinflammatory cytokines and enhances antigen-specific transforming growth factor beta production in antigen-induced arthritis |
| 264 | 1 | a London, UK :b BioMed Central,c 2013 |
| 338 | a electronic2 rdacarrier | |
| 520 | a Introduction: Interferon alpha (IFN-α) has a complex role in autoimmunity, in that it may both enhance and prevent inflammation. We have previously shown that the presence of IFN-α at sensitization protects against subsequent antigen-triggered arthritis. To understand this tolerogenic mechanism, we performed a descriptive, hypothesis-generating study of cellular and humoral responses associated with IFN-α-mediated protection against arthritis.Methods: Arthritis was evaluated at day 28 in mice given a subcutaneous injection of methylated bovine serum albumin (mBSA), together with Freund adjuvant and 0 to 5,000 U IFN-α at days 1 and 7, followed by intraarticular injection of mBSA alone at day 21. The effect of IFN-α on mBSA-specific IgG1, IgG2a, IgG2b, IgA, and IgE was evaluated by enzyme-linked immunosorbent assay (ELISA). Cytokines in circulation and in ex vivo cultures on mBSA restimulation was evaluated with ELISA and Luminex, and the identity of cytokine-producing cells by fluorescence-activated cell sorting (FACS) analysis.Results: Administration of IFN-α protected mice from arthritis in a dose-dependent manner but had no effect on antigen-specific antibody levels. However, IFN-α did inhibit the initial increase of IL-6, IL-10, IL-12, and TNF, and the recall response induced by intraarticular mBSA challenge of IL-1β, IL-10, IL-12, TNF, IFN-γ, and IL-17 in serum. IFN-α decreased both macrophage and CD4+ T cell-derived IFN-γ production, whereas IL-17 was decreased only in CD4+ T cells. Ex vivo, in mBSA-restimulated spleen and lymph node cell cultures, the inhibitory effect of in vivo administration of IFN-α on proinflammatory cytokine production was clearly apparent, but had a time limit. An earlier macrophage-derived, and stronger activation of the antiinflammatory cytokine transforming growth factor beta (TGF-β) was observed in IFN-α-treated animals, combined with an increase in CD4+ T cells producing TGF-β when arthritis was triggered by mBSA (day 21). Presence of IFN-α at immunizations also prevented the reduction in TGF-β production, which was induced by the intraarticular mBSA injection triggering arthritis in control animals.Conclusions: Administration of IFN-α has a profound effect on the cellular response to mBSA plus adjuvant, but does not affect antigen-specific Ig production. By including IFN-α at immunizations, spleen and lymph node cells inhibit their repertoire of antigen-induced proinflammatory cytokines while enhancing antiinflammatory TGF-β production, first in macrophages, and later also in CD4+ T cells. On intraarticular antigen challenge, this antiinflammatory state is reenforced, manifested as inhibition of proinflammatory recall responses and preservation of TGF-β levels. This may explain why IFN-α protects against antigen-induced arthritis. © 2013 Chalise et al.; licensee BioMed Central Ltd. | |
| 700 | 1 | a Narendra, Sudeep Chennau Linköpings universitet,Avdelningen för inflammationsmedicin,Hälsouniversitetet4 aut0 (Swepub:liu)sudch29 |
| 700 | 1 | a Paudyal, Bhesh Raju Linköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet4 aut |
| 700 | 1 | a Magnusson, Mattiasu Linköpings universitet,Avdelningen för inflammationsmedicin,Hälsouniversitetet4 aut0 (Swepub:liu)matma88 |
| 710 | 2 | a Linköpings universitetb Avdelningen för inflammationsmedicin4 org |
| 773 | 0 | t Arthritis Research and Therapyd London, UK : BioMed Centralg 15:5, s. R143-q 15:5<R143-x 1478-6354 |
| 856 | 4 | u https://liu.diva-portal.org/smash/get/diva2:677167/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print |
| 856 | 4 | u https://arthritis-research.biomedcentral.com/track/pdf/10.1186/ar4326 |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-102367 |
| 856 | 4 8 | u https://doi.org/10.1186/ar4326 |
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