Immunotherapy for the prevention and treatment of type 1 diabetes

被引:32
作者
Goudy, KS [1 ]
Tisch, R [1 ]
机构
[1] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
关键词
antigen; autoimmunity; diabetes; T cells;
D O I
10.1080/08830180500379721
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
A major effort has been on-going to develop immunotherapies to prevent and/or treat type 1 diabetes (T1D). This autoimmune disease is characterized by the selective loss of the insulin-producing beta cells via the cumulative effects of autoantigen-specific CD4+ and CD8+ T cells, autoantibodies, and activated antigen-presenting cells. To be applicable in a clinical setting, immunotherapies must suppress established beta-cell autoimmunity. Preclinical studies and recent clinical findings suggest that antigen-specific and systemic-based strategies can be effective in this regard. However, either approach alone may not be sufficient to block the diabetogenic response and establish long-term protection in the clinic. In this review, we will discuss the importance of both strategies and how a combinatorial approach to treat T1D is appealing.
引用
收藏
页码:307 / 326
页数:20
相关论文
共 88 条
[1]   Spontaneous peripheral T-cell responses to the IA-2β (phogrin) autoantigen in young nonobese diabetic mice [J].
Achenbach, P ;
Kelemen, K ;
Wegmann, DR ;
Hutton, JC .
JOURNAL OF AUTOIMMUNITY, 2002, 19 (03) :111-116
[2]   Tolerogenic dendritic cells induced by vitamin D receptor ligands enhance regulatory T cells inhibiting allograft rejection and autoimmune diseases [J].
Adorini, L ;
Penna, G ;
Giarratana, N ;
Uskokovic, M .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2003, 88 (02) :227-233
[3]   Immunological characterization and therapeutic activity of an altered-peptide ligand, NBI-6024, based on the immunodominant type 1 diabetes autoantigen insulin B-chain (9-23) peptide [J].
Alleva, DG ;
Gaur, A ;
Jin, LP ;
Wegmann, D ;
Gottlieb, PA ;
Pahuja, A ;
Johnson, EB ;
Motheral, T ;
Putnam, A ;
Crowe, PD ;
Ling, N ;
Boehme, SA ;
Conlon, PJ .
DIABETES, 2002, 51 (07) :2126-2134
[4]   The NOD mouse: A model of immune dysregulation [J].
Anderson, MS ;
Bluestone, JA .
ANNUAL REVIEW OF IMMUNOLOGY, 2005, 23 :447-485
[5]   Checkpoints in the progression of autoimmune disease: Lessons from diabetes models [J].
Andre, I ;
Gonzalez, A ;
Wang, B ;
Katz, J ;
Benoist, C ;
Mathis, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (06) :2260-2263
[6]   Autoreactive T cell responses show proinflammatory polarization in diabetes but a regulatory phenotype in health [J].
Arif, S ;
Tree, TI ;
Astill, TP ;
Tremble, JM ;
Bishop, AJ ;
Dayan, CM ;
Roep, BO ;
Peakman, M .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 113 (03) :451-463
[7]   IL-10 is a key cytokine in psoriasis -: Proof of principle by IL-10 therapy:: A new therapeutic approach [J].
Asadullah, K ;
Sterry, W ;
Stephanek, K ;
Jasulaitis, D ;
Leupold, M ;
Audring, H ;
Volk, HD ;
Döcke, WD .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (04) :783-794
[8]   TGF-β-dependent mechanisms mediate restoration of self-tolerance induced by antibodies to CD3 in overt autoimmune diabetes [J].
Belghith, M ;
Bluestone, JA ;
Barriot, S ;
Mégret, J ;
Bach, JF ;
Chatenoud, L .
NATURE MEDICINE, 2003, 9 (09) :1202-1208
[9]   Immunology - Selection for survival? [J].
Benoist, C ;
Mathis, D .
SCIENCE, 1997, 276 (5321) :2000-2001
[10]   Encephalitogenic potential of the myelin basic protein peptide (amino acids 83-99) in multiple sclerosis: Results of a phase II clinical trial with an altered peptide ligand [J].
Bielekova, B ;
Goodwin, B ;
Richert, N ;
Cortese, I ;
Kondo, T ;
Afshar, G ;
Gran, B ;
Eaton, J ;
Antel, J ;
Frank, JA ;
McFarland, HF ;
Martin, R .
NATURE MEDICINE, 2000, 6 (10) :1167-1175