Abstract
We have recently reported that lymphocyte activation gene-3 (LAG-3,CD223) mediates the alternative, IFNα-deficient activation of plasmacytoid dendritic cells (pDCs) at tumor sites. Our findings define a novel tumor-driven strategy that promotes immunosuppression by pDCs, and we have provided more detailed information regarding the immunomodulatory role of of LAG-3. The translational relevance of our results for the treatment of tumors and autoimmune diseases is discussed herein.