Specific deletion of autoreactive T cells by adenovirus-transfected, Fas ligand-producing antigen-presenting cells

Zhang, Huang-Ge and Mountz, John D. and Fleck, Martin and Zhou, Tong and Hsu, Hui-Chen (2002) Specific deletion of autoreactive T cells by adenovirus-transfected, Fas ligand-producing antigen-presenting cells. IMMUNOLOGIC RESEARCH, 26 (1-3). pp. 235-246. ISSN 0257-277X

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Abstract

immune privilege is a unique strategy developed in several internal organs that can prevent the development of immune attack against these vital organs. One critical mechanism of immune privilege is utilization of Fas/FasL-mediated apoptosis to delete the invading T cells at the immune privilege sites. In this article, we describe the development and application of a unique cell-gene therapy to correct defective FasL-mediated apoptosis and autoimmune disease in autoimmune mice. This cell-gene therapy strategy using antigen-presenting cells (APCs) to express FasL is not only a therapeutic tool, but also has allowed us to understand the complexity of T cell regulation and the concept of eliminating T cells in the spleen, lymph node, or elsewhere in vivo to regulate the homeostasis of the peripheral T cell response. In this regard, the FasL-expressing APCs can be considered as circulating and regulatable immune privilege sites. Our studies provide substantial evidence that FasL-expressing APCs can be introduced exogenously without liver toxicity to eliminate infiltrating T cells and prevent the development of immune attack in lung, liver, kidney, joint, and salivary gland. Therefore, given the hazardous potential of persistent T cell invasion at the local inflammatory site, it is tempting to speculate that such an endogenous control mechanism occurs normally in vivo to limit a chronic T cell inflammatory response.

Item Type: Article
Uncontrolled Keywords: MARGINAL-ZONE MACROPHAGES; HERPES-SIMPLEX VIRUS; IMMUNE PRIVILEGE; SJOGRENS-SYNDROME; MEDIATED APOPTOSIS; ALLOGRAFT SURVIVAL; UP-REGULATION; CD95 LIGAND; IN-VIVO; EXPRESSION; Fas ligand; antigen-presenting cells; T cells; immune privilege; autoimmune disease
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin I
Depositing User: Dr. Gernot Deinzer
Date Deposited: 16 Nov 2021 07:16
Last Modified: 16 Nov 2021 07:16
URI: https://pred.uni-regensburg.de/id/eprint/40749

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