CD8+T Cells in Type 1 Diabetes

被引:101
作者
Tsai, Sue [1 ]
Shameli, Afshin
Santamaria, Pere
机构
[1] Univ Calgary, JMDRC, Dept Microbiol & Infect Dis, Calgary, AB, Canada
来源
ADVANCES IN IMMUNOLOGY: IMMUNOPATHOGENESIS OF TYPE 1 DIABETES MELLITUS, VOL 100 | 2008年 / 100卷
基金
加拿大健康研究院; 加拿大自然科学与工程研究理事会;
关键词
D O I
10.1016/S0065-2776(08)00804-3
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 (TID), an autoimmune disease once thought to be mediated exclusively by beta cell-specific CD4+ T cells, is now recognized as one in which autoreactive CD8+ T cells play a fundamental role. in the nonobese diabetic (NOD) mouse model, CD8+ T effector cells take centre stage in the destruction of pancreatic beta cells and contribute to sustaining islet inflammation. Recent investigations have elucidated the mechanisms underlying the activation, homing, and beta cell destructive properties of this type of cells. Another important area is the development and testing of novel preemptive or therapeutic "vaccines" that, by targeting effector and/or regulatory autoreactive CD8+ T cell specificities may be able to induce immunological tolerance to beta cells. in humans, our understanding of the role of CD8+ T cells in TID is also growing, through genetic linkage analyses, as welt as epitope identification and characterization of disease-relevant CD8+ T cell responses in patient blood samples. The following review discusses these important advances and how they can converge towards the goal of developing an antigen-specific immunotherapy for T-ID.
引用
收藏
页码:79 / 124
页数:46
相关论文
共 210 条
[1]   THE 1ST EXTERNAL DOMAIN OF THE NONOBESE DIABETIC MOUSE CLASS-II I-A BETA-CHAIN IS UNIQUE [J].
ACHAORBEA, H ;
MCDEVITT, HO .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (08) :2435-2439
[2]   Autoantibodies to IA-2β improve diabetes risk assessment in high-risk relatives [J].
Achenbach, P. ;
Bonifacio, E. ;
Williams, A. J. K. ;
Ziegler, A. G. ;
Gale, E. A. M. ;
Bingley, P. J. .
DIABETOLOGIA, 2008, 51 (03) :488-492
[3]   PEPTIDE-INDUCED T-CELL TOLERANCE TO PREVENT AUTOIMMUNE DIABETES IN A TRANSGENIC MOUSE MODEL [J].
AICHELE, P ;
KYBURZ, D ;
OHASHI, PS ;
ODERMATT, B ;
ZINKERNAGEL, RM ;
HENGARTNER, H ;
PIRCHER, H .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (02) :444-448
[4]   Dendritic cells acquire antigen from apoptotic cells and induce class I restricted CTLs [J].
Albert, ML ;
Sauter, B ;
Bhardwaj, N .
NATURE, 1998, 392 (6671) :86-89
[5]   Transgenic expression of dominant-negative fas-associated death domain protein in β cells protects against fas ligand-induced apoptosis and reduces spontaneous diabetes in nonobese diabetic mice [J].
Allison, J ;
Thomas, HE ;
Catterall, T ;
Kay, TWH ;
Strasser, A .
JOURNAL OF IMMUNOLOGY, 2005, 175 (01) :293-301
[6]   Mechanisms of β cell death in diabetes:: A minor role for CD95 [J].
Allison, J ;
Strasser, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (23) :13818-13822
[7]   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
[8]   Perforin-independent β-cell destruction by diabetogenic CD8+ T lymphocytes in transgenic nonobese diabetic mice [J].
Amrani, A ;
Verdaguer, J ;
Anderson, B ;
Utsugi, T ;
Bou, S ;
Santamaria, P .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 103 (08) :1201-1209
[9]   IL-1α, IL-1β, and IFN-γ mark β cells for Fas-dependent destruction by diabetogenic CD4+ T lymphocytes [J].
Amrani, A ;
Verdaguer, J ;
T'hiessen, S ;
Bou, S ;
Santamaria, P .
JOURNAL OF CLINICAL INVESTIGATION, 2000, 105 (04) :459-468
[10]   CD154-dependent priming of diabetogenic CD4+ T cells dissociated from activation of antigen-presenting cells [J].
Amrani, A ;
Serra, P ;
Yamanouchi, J ;
Han, BY ;
Thiessen, S ;
Verdaguer, J ;
Santamaria, P .
IMMUNITY, 2002, 16 (05) :719-732