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Proceedings Paper

Photodynamic therapy stimulates anti-tumor immunity in a murine mastocytoma model
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Paper Abstract

Photodynamic therapy (PDT) involves the IV administration of photosensitizers followed by illumination of the tumor with red light producing reactive oxygen species that eventually cause vascular shutdown and tumor cell apoptosis. Anti-tumor immunity is stimulated after PDT due to the acute inflammatory response, recognition of tumor-specific antigens, and induction of heat-shock proteins, while the three commonest cancer therapies (surgery, chemotherapy and radiotherapy) all tend to suppress the immune system. Like many other immunotherapies, the extent of the immune response after PDT tends to depend on the antigenicity of the particular tumor, or in other words, whether the tumor contains proteins with the correct characteristics to provide peptides that can bind to MHC class I molecules and provide a target for cytolytic T lymphocytes. We have described certain mouse tumors containing defined or naturally occurring tumor associated antigens that respond particularly well to PDT, and potent immune responses capable of destroying distant untreated tumors can be induced. In this report we address the induction of immunity after PDT of the DBA2 mastocytoma known as P815. This tumor was the first mouse tumor to be shown to possess a tumor-rejection antigen capable of being recognized by cytotoxic T-cells.

Paper Details

Date Published: 18 February 2008
PDF: 9 pages
Proc. SPIE 6857, Biophotonics and Immune Responses III, 685706 (18 February 2008); doi: 10.1117/12.764922
Show Author Affiliations
Pawel Mroz, Wellman Ctr. for Photomedicine, Massachusetts General Hospital (United States)
Harvard Medical School (United States)
Michael R. Hamblin, Wellman Ctr. for Photomedicine, Massachusetts General Hospital (United States)
Harvard Medical School (United States)
Harvard-MIT Division of Health Sciences and Technology (United States)

Published in SPIE Proceedings Vol. 6857:
Biophotonics and Immune Responses III
Wei R. Chen, Editor(s)

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