Specific deletion of autoreactive T cells by adenovirus-transfected, fas ligand-producing antigen-presenting cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-08

AUTHORS

Huang-Ge Zhang, John D. Mountz, Martin Fleck, Tong Zhou, Hui-Chen Hsu

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 utilizati 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, orelse where 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. More... »

PAGES

235-246

Identifiers

URI

http://scigraph.springernature.com/pub.10.1385/ir:26:1-3:235

DOI

http://dx.doi.org/10.1385/ir:26:1-3:235

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1042078966

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12403361


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