Researches at Washington University School of Medicine in St. Louis and St. Jude’s Children’s Research Hospital in Memphis have uncovered new research into cell death and immunity. It has been known for a long time that cells undergo two different types of death, and that one triggers the immune response and the other does not. Programmed cell death, as in what happens when we lose and regrow skin cells does not normally trigger the immune response. Cells that die due to damage or infection trigger the body’s immune system in order to fight and/or repair the damage. It was long believed that the immune response was triggered by the release of HMGB1 from the cell as it was dying from damage or infection and that regular cells did not release this chemical. This new research shows that both types of cell death release HMGB1, but in the case of regular, programmed cell death, the body neutralizes the action of HMGB1 by combining it with free radicals, thereby preventing the immune response.
There are implications for this research in both the treatment of cancer and autoimmune diseases. In the case of cancer, this immune reponse can be stimulated by adding more of this chemical, thereby causing the immune system to attack the cancer. In the case of autoimmune disease where the body attacks itself, the addition of free radicals may counteract the autoimmune response. This is an exciting new development in both cancer and autoimmune disease treatment indeed.
The diagram shown here is progression of normal cells into cancer cells, where programmed cell death is eliminated and diseased cells are allowed to proliferate.
This article was published in the July 18, 2008 issue of Immunity.
Here is a link to the full press release.