Tolerogenic dendritic cells induce antigen-specific hyporesponsiveness in insulin- and glutamic acid decarboxylase 65-autoreactive T lymphocytes from type 1 diabetic patients

Copyright © 2014 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 154(2014), 1 vom: 21. Sept., Seite 72-83
1. Verfasser: Segovia-Gamboa, Norma (VerfasserIn)
Weitere Verfasser: Rodríguez-Arellano, Martha Eunice, Rangel-Cruz, Rafael, Sánchez-Díaz, Moisés, Ramírez-Reyes, Julio César, Faradji, Raquel, González-Domínguez, Érika, Sánchez-Torres, Carmen
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2014
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Dendritic cells Effector/memory CD4+ T lymphocytes; Tolerance; Type 1 diabetes mellitus; Autoantigens Insulin Peptide Fragments glutamate decarboxylase 65 (202-221) mehr... EC 4.1.1.- Glutamate Decarboxylase EC 4.1.1.15
LEADER 01000naa a22002652 4500
001 NLM239794931
003 DE-627
005 20231224120729.0
007 cr uuu---uuuuu
008 231224s2014 xx |||||o 00| ||eng c
024 7 |a 10.1016/j.clim.2014.06.009  |2 doi 
028 5 2 |a pubmed24n0799.xml 
035 |a (DE-627)NLM239794931 
035 |a (NLM)24993292 
035 |a (PII)S1521-6616(14)00156-9 
040 |a DE-627  |b ger  |c DE-627  |e rakwb 
041 |a eng 
100 1 |a Segovia-Gamboa, Norma  |e verfasserin  |4 aut 
245 1 0 |a Tolerogenic dendritic cells induce antigen-specific hyporesponsiveness in insulin- and glutamic acid decarboxylase 65-autoreactive T lymphocytes from type 1 diabetic patients 
264 1 |c 2014 
336 |a Text  |b txt  |2 rdacontent 
337 |a ƒaComputermedien  |b c  |2 rdamedia 
338 |a ƒa Online-Ressource  |b cr  |2 rdacarrier 
500 |a Date Completed 30.09.2014 
500 |a Date Revised 20.11.2014 
500 |a published: Print-Electronic 
500 |a Citation Status MEDLINE 
520 |a Copyright © 2014 Elsevier Inc. All rights reserved. 
520 |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 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Dendritic cells 
650 4 |a Effector/memory CD4+ T lymphocytes; 
650 4 |a Tolerance; 
650 4 |a Type 1 diabetes mellitus; 
650 7 |a Autoantigens  |2 NLM 
650 7 |a Insulin  |2 NLM 
650 7 |a Peptide Fragments  |2 NLM 
650 7 |a glutamate decarboxylase 65 (202-221)  |2 NLM 
650 7 |a EC 4.1.1.-  |2 NLM 
650 7 |a Glutamate Decarboxylase  |2 NLM 
650 7 |a EC 4.1.1.15  |2 NLM 
700 1 |a Rodríguez-Arellano, Martha Eunice  |e verfasserin  |4 aut 
700 1 |a Rangel-Cruz, Rafael  |e verfasserin  |4 aut 
700 1 |a Sánchez-Díaz, Moisés  |e verfasserin  |4 aut 
700 1 |a Ramírez-Reyes, Julio César  |e verfasserin  |4 aut 
700 1 |a Faradji, Raquel  |e verfasserin  |4 aut 
700 1 |a González-Domínguez, Érika  |e verfasserin  |4 aut 
700 1 |a Sánchez-Torres, Carmen  |e verfasserin  |4 aut 
773 0 8 |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 
773 1 8 |g volume:154  |g year:2014  |g number:1  |g day:21  |g month:09  |g pages:72-83 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2014.06.009  |3 Volltext 
912 |a GBV_USEFLAG_A 
912 |a SYSFLAG_A 
912 |a GBV_NLM 
912 |a GBV_ILN_11 
912 |a GBV_ILN_24 
912 |a GBV_ILN_350 
951 |a AR 
952 |d 154  |j 2014  |e 1  |b 21  |c 09  |h 72-83