A purine metabolic checkpoint that prevents autoimmunity and autoinflammation
Svetlana Saveljeva, Gavin W. Sewell, Katharina Ramshorn, M. Zaeem Cader, James A. West, Simon Clare, Lea-Maxie Haag, Rodrigo Pereira de Almeida Rodrigues, Lukas Unger, Ana Belén Iglesias-Romero, Lorraine M. Holland, Christophe Bourges, Muhammad N. Md-Ibrahim, James O. Jones, Richard S. Blumberg, James Lee, Nicole C. Kaneider, Trevor D. Lawley, Allan Bradley, Gordon Dougan, Arthur Kaser
Abstract
-dependent manner by balancing flux through adenine-guanine nucleotide interconversion cycles. FAMIN additionally converts hypoxanthine into inosine, which DCs release to dampen T cell activation. Compromised FAMIN consequently enhances immunosurveillance of syngeneic tumors. FAMIN is a biochemical checkpoint that protects against excessive antiviral T cell responses, autoimmunity, and autoinflammation.