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Fast track to vascular disease
Date:6/3/2011

cells.

In further experiments, the researchers destroyed the T cells of normal mice and replaced them with T cells from the CCL17-deficient mice. Conversely, regulatory T cells were specifically removed from CCL17-deficient mice. "The results of these investigations led us to conclude that CCL17 drives atherosclerosis by inhibiting an important regulatory circuit that acts to restrain the immune response," says Weber. Under normal circumstances, immune reactions are attenuated by regulatory T cells (Tregs) that inhibit other types of immune cells and so ensure that the whole system returns to a balanced state. The new study shows that, in the presence of CCL17, fewer Tregs in the inflamed tissue are activated. In effect, CCL17 disables the Treg-dependent braking mechanism.

"This finding makes CCL17 a promising target for new therapeutic approaches," says Weber, who is anxious to ensure that the results of basic research are transferred as quickly as possible into the clinical setting and find practical medical application. In this case, the first step has already been taken. Using an antibody against CCL17, the authors of the new study were able to block the action of the signal and prevent the progression of atherosclerosis. CCL17 therefore offers a possible handle for new approaches to treatment of the condition. In the next step, Weber and his colleagues hope to clarify the function of the CCL17 receptors on the plasma membrane of the regulatory T cells. (gd)


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Contact: Dr. Christian Weber
kreislaufinstitut@med.uni-muenchen.de
49-895-160-4350
Ludwig-Maximilians-Universitt Mnchen
Source:Eurekalert

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