COX-2 Helps Cancer Cells Avoid Immune Attack

However, in the current study published in the October 1, 2004, issue of the Journal of Immunology, investigators at the Maxine Dunitz Neurosurgical Institute of Cedars-Sinai Medical Center (Los Angeles, CA, USA; www.cedars-sinai.edu/mdnsi) reported that overexpression of COX-2 modified dendritic cell behavior.

When dendritic cells were exposed to cancer cells whose COX-2 overexpression caused elevated levels of prostaglandin E2, the dendritic cells prompted the overproduction of interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta) instead of inducing the production of interleukin-12 (IL-12). These two substances triggered a Trl regulatory response that caused lymphocytes to be tolerant of tumor cell antigens.

Senior author Dr. John S. Yu, co-director of the comprehensive brain tumor program at the Maxine Dunitz Neurosugical Institute, said, "COX-2 expression by tumors may make them invisible to the immune system. By using COX-2 inhibitors, these tumors may become more detectable and therefore more vulnerable to destruction by the immune system. One of the intriguing findings was that helper cells isolated from the bloodstream of a glioblastoma patient predominantly displayed a regulatory response against the patient's glioma cells. This points to the existence of an underlying regulatory bias in the circulating T cells of patients with malignant glioma.”




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