Targeted depletion of lymphotoxin-alpha-expressing TH1 and TH17 cells inhibits autoimmune disease.

B cell–depleting antibodies have therapeutic efficacy against arthritis. Here Jane Grogan and her colleagues report a new approach to depleting pathogenic T cells. They show that lymphotoxin-α is upregulated on the surface of activated TH1 and TH17 CD4+ cells, which have a pathogenic role in several autoimmune diseases, and a monoclonal antibody targeted to lymphotoxin-a can inhibit collagen-induced arthritis and EAE in mice (pages 732–733).