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Decreased dendritic cell numbers but increased TLR9-mediated interferon-alpha production in first degree relatives of type 1 diabetes patients
J. Kayserova, J. Vcelakova, K. Stechova, E. Dudkova, H. Hromadkova, Z. Sumnik, S. Kolouskova, R. Spisek, A. Sediva,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NT11407
MZ0
CEP - Centrální evidence projektů
- MeSH
- dendritické buňky imunologie metabolismus MeSH
- diabetes mellitus 1. typu imunologie metabolismus MeSH
- dítě MeSH
- dospělí MeSH
- interferon alfa biosyntéza krev MeSH
- leukocyty mononukleární účinky léků metabolismus MeSH
- lidé MeSH
- ligandy MeSH
- mladiství MeSH
- mladý dospělý MeSH
- oligodeoxyribonukleotidy farmakologie MeSH
- počet buněk MeSH
- předškolní dítě MeSH
- rodina MeSH
- toll-like receptor 9 metabolismus MeSH
- Check Tag
- dítě MeSH
- dospělí MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
OBJECTIVE: Dendritic cells (DCs) play an important role in pathogenesis of autoimmunity, including type 1 diabetes (T1D). In this study, we investigated DC subpopulations and their responses to TLR stimulation in T1D patients and their relatives. METHODS: We analyzed the frequency of myeloid (mDCs) and plasmacytoid DCs (pDCs) in 97 T1D patients (69 onset, 28 long-term), 67 first-degree relatives, and 64 controls. We additionally tested the IFN-alpha production by pDCs upon stimulation with TLR 7, 8 and 9 agonists. RESULTS: A lower number of mDCs and pDCs were found in T1D patients and their relatives. Of all the tested TLR ligands, only stimulation with CpG 2216 induced IFN-alpha production that was the highest in T1D relatives, except of autoantibody-negative relatives bearing the protective haplotypes. CONCLUSION: Our data demonstrate disturbances in DC number and function expressed most significantly in T1D relatives and point to a potential role of TLR9-induced IFN-alpha production in T1D development.
Citace poskytuje Crossref.org
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- $a Kayserova, Jana $u Department of Immunology, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: jana.kayserova@lfmotol.cuni.cz.
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- $a Decreased dendritic cell numbers but increased TLR9-mediated interferon-alpha production in first degree relatives of type 1 diabetes patients / $c J. Kayserova, J. Vcelakova, K. Stechova, E. Dudkova, H. Hromadkova, Z. Sumnik, S. Kolouskova, R. Spisek, A. Sediva,
- 520 9_
- $a OBJECTIVE: Dendritic cells (DCs) play an important role in pathogenesis of autoimmunity, including type 1 diabetes (T1D). In this study, we investigated DC subpopulations and their responses to TLR stimulation in T1D patients and their relatives. METHODS: We analyzed the frequency of myeloid (mDCs) and plasmacytoid DCs (pDCs) in 97 T1D patients (69 onset, 28 long-term), 67 first-degree relatives, and 64 controls. We additionally tested the IFN-alpha production by pDCs upon stimulation with TLR 7, 8 and 9 agonists. RESULTS: A lower number of mDCs and pDCs were found in T1D patients and their relatives. Of all the tested TLR ligands, only stimulation with CpG 2216 induced IFN-alpha production that was the highest in T1D relatives, except of autoantibody-negative relatives bearing the protective haplotypes. CONCLUSION: Our data demonstrate disturbances in DC number and function expressed most significantly in T1D relatives and point to a potential role of TLR9-induced IFN-alpha production in T1D development.
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- $a Vcelakova, Jana $u Department of Pediatrics, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: jana.vcelakova@lfmotol.cuni.cz.
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- $a Stechova, Katerina $u Department of Pediatrics, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: katerina.stechova@lfmotol.cuni.cz.
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- $a Dudkova, Eva $u Department of Immunology, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: eva.dudkova@fnmotol.cz.
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- $a Hromadkova, Hana $u Department of Immunology, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: hana.hromadkova@lfmotol.cuni.cz.
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- $a Sumnik, Zdenek $u Department of Pediatrics, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: zdenek.sumnik@lfmotol.cuni.cz.
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- $a Kolouskova, Stanislava $u Department of Pediatrics, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: stanislava.kolouskova@lfmotol.cuni.cz.
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- $a Spisek, Radek $u Department of Immunology, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic; Sotio a.s., Jankovcova 2, Prague, Czech Republic. Electronic address: spisek@sotio.com.
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- $a Sediva, Anna $u Department of Immunology, Charles University, 2nd Faculty of Medicine, University Hospital Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: anna.sediva@fnmotol.cz.
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- $w MED00005218 $t Clinical immunology (Orlando, Fla.) $x 1521-7035 $g Roč. 153, č. 1 (2014), s. 49-55
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