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Proceedings Article

Molecular mechanism of PDT-induced apoptotic cells stimulation NO production in macrophages

[+] Author Affiliations
Sheng Song, Fei-fan Zhou, Si-hua Yang

South China Normal Univ. (China)

Wei R. Chen

South China Normal Univ. (China) and Univ. of Central Oklahoma (USA)

Proc. SPIE 7900, Biophotonics and Immune Responses VI, 790008 (February 10, 2011); doi:10.1117/12.874324
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From Conference Volume 7900

  • Biophotonics and Immune Responses VI
  • Wei R. Chen
  • San Francisco, California, USA | January 22, 2011

abstract

It is well known that apoptotic cells (AC) participate in immune response. The immune response induced by AC, either immunostimulatory or immunosuppressive, have been extensively studied. However, the molecular mechanisms of the immunostimulatory effects induced by PDT-treated AC remain unclear. Nitric oxide (NO) is an important signal transduction molecule and has been implicated in a variety of functions. It has also been found to play an important role not only as a cytotoxic effector but an immune regulatory mediator. In this study, we demonstrate that the PDT-induced apoptotic tumor cells stimulate the production of NO in macrophages by up-regulating expression of inducible nitric oxide synthase (iNOS). In addition, we show that AC, through toll-like receptors (TLRs), can activate myeloid differentiation factor-88 (MyD88), indicating that AC serves as an intercellular signal to induce iNOS expression in immune cells after PDT treatment. This study provided more details for understanding the molecular mechanism of the immune response induced by PDT-treated AC.

© (2011) COPYRIGHT Society of Photo-Optical Instrumentation Engineers (SPIE). Downloading of the abstract is permitted for personal use only.

Topics

Molecules ; NOx
Citation

Sheng Song ; Fei-fan Zhou ; Si-hua Yang and Wei R. Chen
"Molecular mechanism of PDT-induced apoptotic cells stimulation NO production in macrophages", Proc. SPIE 7900, Biophotonics and Immune Responses VI, 790008 (February 10, 2011); doi:10.1117/12.874324; http://dx.doi.org/10.1117/12.874324


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