Immunotherapy of type 1 diabetes

被引：11

作者：

Li, Li ^{[1
]}

Yi, Zuoan ^{[1
]}

Tisch, Roland ^{[1
]}

Wang, Bo ^{[1
]}

机构：

[1] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA

来源：

ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS | 2008年 / 56卷 / 04期

基金：

美国国家卫生研究院;

关键词：

antibody; antigen-specific; immunoregulatory T cells; tolerance;

D O I：

10.1007/s00005-008-0025-2

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Type 1 diabetes (T1D) is an autoimmune disease in which the insulin-producing beta cells are destroyed. Diabetic patients manage their hyperglycemia by daily insulin injections. However, insulin therapy is by no means a cure. Accordingly, a significant effort has been ongoing to develop immunotherapies that effectively prevent and/or treat T1D in the clinic. This review focuses on antigen- and antibody-based immunotherapies and discusses the respective strengths and weaknesses of these approaches.

引用

页码：227 / 236

页数：10

共 128 条

[1] Clinical evidence for the safety of GAD65 immunomodulation in adult-onset autoimmune diabetes [J].

Agardh, CD ;

Cilio, CM ;

Lethagen, Å ;

Lynch, K ;

Leslie, RDG ;

Palmér, M ;

Harris, RA ;

Robertson, JA ;

Lernmark, Å .

JOURNAL OF DIABETES AND ITS COMPLICATIONS, 2005, 19 (04) :238-246

[2]

ALEGRE ML, 1994, TRANSPLANTATION, V57, P1537

[3] Progression of autoimmune diabetes driven by avidity maturation of a T-cell population [J].

Amrani, A ;

Verdaguer, J ;

Serra, P ;

Tafuro, S ;

Tan, RS ;

Santamaria, P .

NATURE, 2000, 406 (6797) :739-742

[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] Insulin gene/IDDM2 locus in Japanese type 1 diabetes:: Contribution of class I alleles and influence of class I subdivision in susceptibility to type 1 diabetes [J].

Awata, Takuya ;

Kawasaki, Eiji ;

Ikegami, Hiroshi ;

Kobayashi, Tetsuro ;

Maruyama, Taro ;

Nakanishi, Koji ;

Shimada, Akira ;

Iizuka, Hiroyuki ;

Kurihara, Susumu ;

Osaki, Masataka ;

Uga, Miho ;

Kawabata, Yumiko ;

Tanaka, Shoichiro ;

Kanazawa, Yasuhiko ;

Katayama, Shigehiro .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2007, 92 (05) :1791-1795

[8] INSULIN-DEPENDENT DIABETES-MELLITUS AS AN AUTOIMMUNE-DISEASE [J].

BACH, JF .

ENDOCRINE REVIEWS, 1994, 15 (04) :516-542

[9] Antigen-specific modulation of experimental myasthenia gravis:: Nasal tolerization with recombinant fragments of the human acetylcholine receptor α-subunit [J].

Barchan, D ;

Souroujon, MC ;

Im, SH ;

Antozzi, C ;

Fuchs, S .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (14) :8086-8091

[10] 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

← 1 2 3 4 5 6 7 8 9 10 →