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Apoptotic and necrotic cells induced by different agents vary in their expression of MHC and costimulatory genes. | LitMetric

Apoptotic and necrotic cells induced by different agents vary in their expression of MHC and costimulatory genes.

Mol Immunol

Department of Immunology, Laboratory of Molecular Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

Published: May 2005

AI Article Synopsis

  • Recent research in a murine tumor model shows that apoptotic cells generated by various agents have different effects on the host immune response, though the reasons are still unclear.
  • The study compared immune gene expression (like MHC class I and II, CD40, B7-1, B7-2) in viable and apoptotic cells induced by four agents, finding that only the histone deacetylase inhibitor TSA increased MHC class II expression.
  • Each agent led to distinct patterns of costimulatory molecules on apoptotic cells, indicating that these variations could impact the tumor's ability to trigger an immune response.

Article Abstract

We have recently reported, in a murine tumor model, that apoptotic cells induced by different agents may vary in their ability to elicit host immunity. The basis for this observation is unclear but may involve varying efficiencies of cross-presentation and/or direct activation of immunity by different apoptotic preparations. As a first step in addressing this issue, we compared expression patterns of selected immune genes (MHC class I, class II, CD40, B7-1, B7-2) on viable and apoptotic populations induced by four different agents. The histone deacetylase inhibitor trichostatin A (TSA) induced MHC class II expression on viable and apoptotic cell populations, while LPAM, H2O2 and gamma-irradiation did not activate class II. Each agent employed elicited a different expression pattern of costimulatory molecules (CD40, B7-1, B7-2) on both apoptotic and 7-AAD+ 'necrotic' populations. In striking contrast to the TSA induction of MHC class II, class I cell surface protein was diminished on the apoptotic populations. These effects were not a result of changes in the cell cycle produced by the various treatments. The data demonstrate that distinctive gene expression patterns on viable and apoptotic cells are elicited by different apoptosis inducing agents. We discuss how expression patterns on dead or dying tumor cells could potentially affect the tumor's ability to elicit immunity.

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Source
http://dx.doi.org/10.1016/j.molimm.2004.09.030DOI Listing

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