(PHILADELPHIA - April 16, 2002) - Scientists know that the potential to generate dangerous antibodies that attack our own cells and tissues - one of the defining characteristics of autoimmune disorders like lupus - exists in everyone. That potential is unrealized in healthy individuals, but spins out of control in those who develop disease. So, what are the factors that push the potential for producing these antibodies into action and cause autoimmunity in some individuals? A new study from researchers at The Wistar Institute suggests that health depends on maintaining a balance of normal, but countervailing processes in the immune system. New approaches to developing treatments for autoimmunity might focus on influencing this balance.

In lupus and other autoimmune diseases, antibodies against our own cells and tissues are produced by B cells. The body contains billions of B cells that can make antibodies that target infecting viruses and bacteria, but these antibodies can also include ones that can react with "self" - an immunologist's term for our own bodies. One process that normally prevents these B cells from causing harm is that their activity depends on receiving "help" from T helper cells that also become stimulated when an infection occurs. However, another kind of T cell, called a regulatory T cell, may be important in preventing T helper cells from activating B cells with the potential to generate self-reactive antibodies.

Under normal circumstances, according to the Wistar study, a critical balance may exist between T helper cells and regulatory T cells. The researchers saw that providing T helper cells to healthy mice could cause autoreactive B cells to become active, and that removing T helper cells could alleviate disease in lupus-prone mice. They also found that regulatory T cells could stop T helper cells from activating the B cells, suggesting that the presence of self-reactive T helper cells with too few regulatory T cells may be
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Contact: Franklin Hoke
hoke@wistar.upenn.edu
215-898-3716
The Wistar Institute
16-Apr-2002

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