Literature DB >> 10471973

Treatment of an autoimmune disease with "classical" T cell veto: a proposal.

U D Staerz1, Y Qi.   

Abstract

Immune responses protect against infectious diseases and cancers. In normal circumstances, the immune system is tolerant to self. However, under certain conditions this tolerance is broken. The immune system attacks otherwise normal tissue. An autoimmune disease ensues. Strategies are now being sought that remove the pathogenic T cells without affecting other immune functions. "Classical" veto has been described as an immune suppressive mechanism able to remove T cells in a highly specific and effective manner. The present article briefly reviews the current knowledge on the development of autoreactive T cells and their regulation in the periphery. It describes "classical" veto, its mechanisms, and its novel applications. Finally, it argues that "classical" veto can be adapted to treat an autoimmune disease, such as type I diabetes mellitus.

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Year:  1999        PMID: 10471973     DOI: 10.1023/a:1020511928974

Source DB:  PubMed          Journal:  J Clin Immunol        ISSN: 0271-9142            Impact factor:   8.317


  92 in total

1.  Fas-based lymphocyte-mediated cytotoxicity against syngeneic activated lymphocytes: a regulatory pathway?

Authors:  F Vignaux; P Golstein
Journal:  Eur J Immunol       Date:  1994-04       Impact factor: 5.532

2.  CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice.

Authors:  R Yoneda; K Yokono; M Nagata; Y Tominaga; H Moriyama; K Tsukamoto; M Miki; N Okamoto; H Yasuda; K Amano; M Kasuga
Journal:  Diabetologia       Date:  1997-09       Impact factor: 10.122

3.  Rapid and long-term changes to host cytotoxic T lymphocyte precursors reactive to donor antigens caused by intravenous injection of histoincompatible lymphocytes.

Authors:  D R Martin; X Sheng-Tanner; R G Miller
Journal:  Transplantation       Date:  1992-07       Impact factor: 4.939

4.  MHC class I-mediated antigen presentation and induction of CD8+ cytotoxic T-cell responses in autoimmune diabetes-prone NOD mice.

Authors:  D V Serreze; W S Gallichan; D P Snider; K Croitoru; K L Rosenthal; E H Leiter; G J Christianson; M E Dudley; D C Roopenian
Journal:  Diabetes       Date:  1996-07       Impact factor: 9.461

5.  Long-term survival of segmental pancreas isografts in NOD/Lt mice treated with anti-CD4 and anti-CD8 monoclonal antibodies.

Authors:  P L Mottram; L J Murray-Segal; W Han; J Maguire; A Stein-Oakley; T E Mandel
Journal:  Diabetes       Date:  1998-09       Impact factor: 9.461

6.  Autoantibodies to protein tyrosine phosphatase-like proteins in type I diabetes. Overlapping specificities to phogrin and ICA512/IA-2.

Authors:  E Kawasaki; G S Eisenbarth; C Wasmeier; J C Hutton
Journal:  Diabetes       Date:  1996-10       Impact factor: 9.461

7.  Induction of class II MHC antigens in vitro on pancreatic B cells isolated from BB/E rats.

Authors:  R Walker; A Cooke; A J Bone; B M Dean; P van der Meide; J D Baird
Journal:  Diabetologia       Date:  1986-10       Impact factor: 10.122

8.  Differential expression of GAD65 and GAD67 in human, rat, and mouse pancreatic islets.

Authors:  J Kim; W Richter; H J Aanstoot; Y Shi; Q Fu; R Rajotte; G Warnock; S Baekkeskov
Journal:  Diabetes       Date:  1993-12       Impact factor: 9.461

9.  Hybrid antibody mediated veto of cytotoxic T lymphocyte responses.

Authors:  Y Qi; R Berg; M A Singleton; J E Debrick; U D Staerz
Journal:  J Exp Med       Date:  1996-05-01       Impact factor: 14.307

10.  Survival of mature CD4 T lymphocytes is dependent on major histocompatibility complex class II-expressing dendritic cells.

Authors:  T Brocker
Journal:  J Exp Med       Date:  1997-10-20       Impact factor: 14.307

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