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Int Rev Immunol. 2005 Sep-Dec;24(5-6):287-305.

Achieving antigen-specific tolerance in diabetes: regulating specifically.

Author information

1
Naomi Berrie Diabetes Center and the Division of Endocrinology, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. kh318@columbia.edu

Erratum in

  • Int Rev Immunol. 2006 Jan-Apr;25(1-2):49.

Abstract

Autoreactive T cells that escape negative selection in the thymus do not normally cause productive immune responses to self-antigens because of a number of regulatory mechanisms. Studies with anti-CD3 monoclonal antibodies (mAbs) have suggested that immune regulatory mechanisms are induced by drug treatments that are able to stop on-going unwanted immune responses, such as type 1 diabetes, involving induction of regulatory T cells. TGF-beta dependent and independent mechanisms have been described involving CD4(+) as well as CD8(+) T cells. The challenge is now to apply these mechanisms in an antigen-specific manner and so that lasting tolerance to the autoimmune responses can be maintained. We discuss recent data concerning the mechanisms of anti-CD3 mAb treatment and the ways in which our understanding of these mechanisms can be used to develop adoptive immune therapy with regulatory T cells to treat patients with type 1 diabetes or other autoimmune diseases.

PMID:
16318983
DOI:
10.1080/08830180500379671
[Indexed for MEDLINE]

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