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231224s2014 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2014.06.009
|2 doi
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|a pubmed24n0799.xml
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|a (DE-627)NLM239794931
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|a (NLM)24993292
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|a (PII)S1521-6616(14)00156-9
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Segovia-Gamboa, Norma
|e verfasserin
|4 aut
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|a Tolerogenic dendritic cells induce antigen-specific hyporesponsiveness in insulin- and glutamic acid decarboxylase 65-autoreactive T lymphocytes from type 1 diabetic patients
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|c 2014
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 30.09.2014
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|a Date Revised 20.11.2014
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2014 Elsevier Inc. All rights reserved.
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|a Tolerogenic dendritic cells (tDC) constitute a promising therapy for autoimmune diseases, since they can anergize T lymphocytes recognizing self-antigens. Patients with type 1 diabetes mellitus (T1D) have autoreactive T cells against pancreatic islet antigens (insulin, glutamic acid decarboxylase 65 -GAD65-). We aimed to determine the ability of tDC derived from T1D patients to inactivate their insulin- and GAD65-reactive T cells. CD14+ monocytes and CD4+CD45RA- effector/memory lymphocytes were isolated from 25 patients. Monocyte-derived DC were generated in the absence (control, cDC) or presence of IL-10 and TGF-β1 (tDC), and loaded with insulin or GAD65. DC were cultured with T lymphocytes (primary culture), and cell proliferation and cytokine secretion were determined. These lymphocytes were rechallenged with insulin-, GAD65- or candidin-pulsed cDC (secondary culture) to assess whether tDC rendered T cells hyporesponsive to further stimulation. In the primary cultures, tDC induced significant lower lymphocyte proliferation and IL-2 and IFN-γ secretion than cDC; in contrast, tDC induced higher IL-10 production. Lymphocytes from 60% of patients proliferated specifically against insulin or GAD65 (group 1), whereas 40% did not (group 2). Most patients from group 1 had controlled glycemia. The secondary cultures showed tolerance induction to insulin or GAD65 in 14 and 10 patients, respectively. A high percentage of these patients (70-80%) belonged to group 1. Importantly, tDC induced antigen-specific T-cell hyporesponsiveness, since the responses against unrelated antigens were unaffected. These results suggest that tDC therapy against multiple antigens might be useful in a subset of T1D patients
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Dendritic cells
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|a Effector/memory CD4+ T lymphocytes;
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|a Tolerance;
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|a Type 1 diabetes mellitus;
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|a Autoantigens
|2 NLM
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|a Insulin
|2 NLM
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|a Peptide Fragments
|2 NLM
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|a glutamate decarboxylase 65 (202-221)
|2 NLM
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|a EC 4.1.1.-
|2 NLM
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|a Glutamate Decarboxylase
|2 NLM
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|a EC 4.1.1.15
|2 NLM
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|a Rodríguez-Arellano, Martha Eunice
|e verfasserin
|4 aut
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|a Rangel-Cruz, Rafael
|e verfasserin
|4 aut
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|a Sánchez-Díaz, Moisés
|e verfasserin
|4 aut
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|a Ramírez-Reyes, Julio César
|e verfasserin
|4 aut
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|a Faradji, Raquel
|e verfasserin
|4 aut
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|a González-Domínguez, Érika
|e verfasserin
|4 aut
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|a Sánchez-Torres, Carmen
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 154(2014), 1 vom: 21. Sept., Seite 72-83
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:154
|g year:2014
|g number:1
|g day:21
|g month:09
|g pages:72-83
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|u http://dx.doi.org/10.1016/j.clim.2014.06.009
|3 Volltext
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|a GBV_ILN_11
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|a GBV_ILN_350
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|a AR
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|d 154
|j 2014
|e 1
|b 21
|c 09
|h 72-83
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