Decreased blood dendritic cell counts in type 1 diabetic children

被引:59
作者
Vuckovic, Slavica
Withers, Geoff
Harris, Mark
Khalil, Dalia
Gardiner, Damien
Flesch, Inge
Tepes, Sonia
Greer, Ristan
Cowley, David
Cotterill, Andrew
Hart, Derek N. J.
机构
[1] Mater Med Res Inst, Brisbane, Qld 4101, Australia
[2] Royal Childrens Hosp Brisbane, Brisbane, Qld, Australia
[3] Mater Childrens Hosp, Endocrinol Dept, Brisbane, Qld, Australia
[4] Mater Adult Hosp, Clin Chem, Brisbane, Qld, Australia
关键词
dendritic cells; type; 1; diabetes; activation; cytokines;
D O I
10.1016/j.clim.2007.03.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In this study DC numbers, phenotype and DC responses to the Toll-like receptor (TLR)-3 ligand, poly I:C, were examined in new-onset Type 1 diabetes (T1D) patients (ND) and in established T1D patients (ED). Absolute blood myeloid DC (MDC) and plasmacytoid DC (PDC) numbers were decreased in ND and ED patients compared to age-matched controls. The decrease in MDC and PDC counts was less evident in patients with a combination of T1D and coeliac disease (CD) or CD alone. The age-dependent decline in blood DC numbers, found in control children, was not evident in ND patients, such that 2-10 years old ND children had similar MDC and PDC numbers to 15-17 years old controls. In ED patients the t-score of MDC and PDC numbers related to the age of diagnosis but not to disease duration. Blood DC in T1D patients were not distinguished from those of controls by the levels of HLA-DR, CD40 and CD86 expression or the percentage of DC expressing cytokines, IL-12, IL-10, IL-6 and TNF-alpha, in responses to poly I:C. If low DC numbers are shown to contribute to the autoimmunity in T1D, interventions aimed to increase DC numbers may mitigate against beta-cell toss. Crown Copyright (C) 2007 Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:281 / 288
页数:8
相关论文
共 23 条
[1]  
Almeida J, 1999, CLIN EXP IMMUNOL, V118, P392
[2]   Altered phenotype and function of dendritic cells in children with type 1 diabetes [J].
Angelini, F ;
Del Duca, E ;
Piccinini, S ;
Pacciani, V ;
Rossi, P ;
Bitti, MLM .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2005, 142 (02) :341-346
[3]   PREVENTION OF DIABETES IN NONOBESE DIABETIC MICE BY DENDRITIC CELL TRANSFER [J].
CLARESALZLER, MJ ;
BROOKS, J ;
CHAI, A ;
VANHERLE, K ;
ANDERSON, C .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (03) :741-748
[4]   Dendritic cells in human thymus and periphery display a proinsulin epitope in a transcription-dependent, capture-independent fashion [J].
Garcia, CA ;
Prabakar, KR ;
Diez, J ;
Cao, ZA ;
Allende, G ;
Zeller, M ;
Dogra, R ;
Mendez, A ;
Rosenkranz, E ;
Dahl, U ;
Ricordi, C ;
Hanahan, D ;
Pugliese, A .
JOURNAL OF IMMUNOLOGY, 2005, 175 (04) :2111-2122
[5]   CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-β-TGF-β receptor interactions in type 1 diabetes [J].
Green, EA ;
Gorelik, L ;
McGregor, CM ;
Tran, EH ;
Flavell, RA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (19) :10878-10883
[6]   Pancreatic lymph node-derived CD4+CD25+ Treg cells:: Highly potent regulators of diabetes that require TRANCE-RANK signals [J].
Green, EA ;
Choi, YW ;
Flavell, RA .
IMMUNITY, 2002, 16 (02) :183-191
[7]   Maintaining the norm: T-CELL homeostasis [J].
Jameson, SC .
NATURE REVIEWS IMMUNOLOGY, 2002, 2 (08) :547-556
[8]   Homeostatic expansion of T cells during immune insufficiency generates autoimmunity [J].
King, C ;
Ilic, A ;
Koelsch, K ;
Sarvetnick, N .
CELL, 2004, 117 (02) :265-277
[9]   Kinetics of dendritic cell activation:: impact on priming of TH1, TH2 and nonpolarized T cells [J].
Langenkamp, A ;
Messi, M ;
Lanzavecchia, A ;
Sallusto, F .
NATURE IMMUNOLOGY, 2000, 1 (04) :311-316
[10]   Myeloid blood CD11c+ dendritic cells and monocyte-derived dendritic cells differ in their ability to stimulate T lymphocytes [J].
Osugi, Y ;
Vuckovic, S ;
Hart, DNJ .
BLOOD, 2002, 100 (08) :2858-2866