A20 controls macrophage to elicit potent cytotoxic CD4(+) T cell response.
Emerging evidence indicates that CD4(+) T cells possess cytotoxic potential for tumor eradication and perforin/granzyme-mediated cytotoxicity functions as one of the important mechanisms for CD4(+) T cell-triggered cell killing. However, the critical issue is how the cytotoxic CD4(+) T cells are dev...
Main Authors: | , , , , , |
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Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2012-01-01
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Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC3492139?pdf=render |
Summary: | Emerging evidence indicates that CD4(+) T cells possess cytotoxic potential for tumor eradication and perforin/granzyme-mediated cytotoxicity functions as one of the important mechanisms for CD4(+) T cell-triggered cell killing. However, the critical issue is how the cytotoxic CD4(+) T cells are developed. During the course of our work that aims at promoting immunostimulation of APCs by inhibition of negative regulators, we found that A20-silenced Mф drastically induced granzyme B expression in CD4(+) T cells. As a consequence, the granzyme-highly expressing CD4(+) T cells exhibited a strong cytotoxic activity that restricted tumor development. We found that A20-silenced Mф activated cytotoxic CD4(+) T cells by MHC class-II restricted mechanism and the activation was largely dependent on enhanced production of IFN-γ. |
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ISSN: | 1932-6203 |