The finding, published in the Aug. 7 online issue of the journal Immunity, may give scientists a new path to pursue in finding ways to stop the immune system's chronic attacks on the body's own tissue during these diseases.

B cells, the source of damaging auto-antibodies, have long been thought to remain quiet in autoimmune diseases unless they are given a kick-start by T-cells. Researchers from Yale and Boston universities had found that toll-like receptors recognize and react to "self" molecules, in particular mammalian DNA and RNA. When this occurs, these receptors help activate B cells that make the classical auto-antibodies of lupus.

These signals, like those from T-cells, start the autoimmune process in B cells. In the new study, the researchers theorize that once activated in this way, the B cells can subsequently recruit T-cells. This creates a "vicious cycle" of chronic autoimmune disease in which the two types of cell prod each other into action.

The findings could explain why autoimmune-disease treatments aimed at T-cells have not done as well as those targeting B cells, the researchers said.

�?Kevin McKeever