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Costimulation and autoimmune diabetes in BB rats

被引：17
作者：
Beaudette-Zlatanova, BC
Whalen, B
Zipris, D
Yagita, H
Rozing, J
Groen, H
Benjamin, CD
Hunig, T
Drexhage, HA
Ansari, MJ
Leif, J
Mordes, JP
Greiner, DL [1 ]
Sayegh, MH
Rossini, AA
机构：
[1] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA 01605 USA
[2] Biomed Res Models Inc, Worcester, MA USA
[3] Juntendo Univ, Sch Med, Dept Immunol, Tokyo 113, Japan
[4] Univ Groningen, Dept Cell Biol, Immunol Sect, Groningen, Netherlands
[5] Biogen Inc, Boston, MA USA
[6] Univ Wurzburg, Inst Virol & Immunobiol, D-8700 Wurzburg, Germany
[7] Erasmus Univ, Med Ctr, Dept Immunol, Rotterdam, Netherlands
[8] Brigham & Womens Hosp, Transplantat Res Ctr, Boston, MA 02115 USA
[9] Childrens Hosp, Boston, MA 02115 USA
[10] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA USA
来源：
AMERICAN JOURNAL OF TRANSPLANTATION | 2006年 / 6卷 / 05期
关键词：
autoimmunity; diabetes; rodent; tolerance; transplantation;
D O I：
10.1111/j.1600-6143.2005.01227.x
中图分类号：
R61 [外科手术学];
学科分类号：
摘要：
Costimulatory signals regulate T-cell activation. To investigate the role of costimulation in autoimmunity and transplantation, we studied the BB rat model of type 1 diabetes. Diabetes-prone BB (BBDP) rats spontaneously develop disease when 55-120 days of age. We observed that two anti-CD28 monoclonal antibodies (mAb) with different functional activities completely prevented diabetes in BBDP rats. Anti-CD154 mAb delayed diabetes, whereas treatment with CTLA4-Ig or anti-CD80 mAb accelerated disease. Anti-CD86 or anti-CD134L mAbs had no effect. Diabetes resistant BB (BBDR) rats are disease-free, but > 95% of them develop diabetes after treatment with polyinosinicpolycytidylic acid and an mAb that depletes Treg cells. In the induced BBDR model, anti-CD154 mAb delayed onset of diabetes, whereas CTLA4-Ig, anti-CD134L or either of the anti-CD28 mAbs had little or no effect. In contrast, blockade of the CD134-CD134L pathway
引用
收藏
页码：894 / 902
页数：9
相关论文
共 71 条
[1]   Heterologous immunity provides a potent barrier to transplantation tolerance [J].
Adams, AB ;
Williams, MA ;
Jones, TR ;
Shirasugi, N ;
Durham, MM ;
Kaech, SM ;
Wherry, EJ ;
Onami, T ;
Lanier, JG ;
Kokko, KE ;
Pearson, TC ;
Ahmed, R ;
Larsen, CP .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (12) :1887-1895
[2]   The chemokine RANTES is a crucial mediator of the progression from acute to chronic colitis in the rat [J].
Ajuebor, MN ;
Hogaboam, GM ;
Kunkel, SL ;
Proudfoot, AEI ;
Wallace, JL .
JOURNAL OF IMMUNOLOGY, 2001, 166 (01) :552-558
[3]   Prolonged survival of neonatal porcine islet xenografts in mice treated with a donor-specific transfusion and anti-CD154 antibody [J].
Appel, MC ;
Banuelos, SJ ;
Greiner, DL ;
Shultz, LD ;
Mordes, JP ;
Rossini, AA .
TRANSPLANTATION, 2004, 77 (09) :1341-1349
[4]   Neonatal activation of CD28 signaling overcomes T cell anergy and prevents autoimmune diabetes by an IL-4-dependent mechanism [J].
Arreaza, GA ;
Cameron, MJ ;
Jaramillo, A ;
Gill, BM ;
Hardy, D ;
Laupland, KB ;
Rapoport, MJ ;
Zucker, P ;
Chakrabarti, S ;
Chensue, SW ;
Qin, HY ;
Singh, B ;
Delovitch, TL .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (09) :2243-2253
[5]   The NOD mouse model of type 1 diabetes: As good as it gets? [J].
Atkinson, MA ;
Leiter, EH .
NATURE MEDICINE, 1999, 5 (06) :601-604
[6]  
Balasa B, 1997, J IMMUNOL, V159, P4620
[7]   Signaling through OX40 (CD134) breaks peripheral T-cell tolerance [J].
Bansal-Pakala, P ;
Jember, AGH ;
Croft, M .
NATURE MEDICINE, 2001, 7 (08) :907-912
[8]   Ligation of OX40 (CD134) regulates graft-versus-host disease (GVHD) and graft rejection in allogeneic bone marrow transplant recipients [J].
Blazar, BR ;
Sharpe, AH ;
Chen, AI ;
Panoskaltsis-Mortari, A ;
Lees, C ;
Akiba, H ;
Yagita, H ;
Killeen, N ;
Taylor, PA .
BLOOD, 2003, 101 (09) :3741-3748
[9]   Levels of Art2+ cells but not soluble Art2 protein correlate with expression of autoimmune diabetes in the BB rat [J].
Bortell, R ;
Waite, DJ ;
Whalen, BJ ;
Todd, D ;
Leif, JH ;
Lesma, E ;
Moss, J ;
Mordes, JP ;
Rossini, AA ;
Greiner, DL .
AUTOIMMUNITY, 2001, 33 (03) :199-211
[10]   Costimulation controls diabetes by altering the balance of pathogenic and regulatory T cells [J].
Bour-Jordan, H ;
Salomon, BL ;
Thompson, HL ;
Szot, GL ;
Bernhard, MR ;
Bluestone, JA .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (07) :979-987
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