HAVCR2 and autoimmune disease: TIM-3 can be shed from the cell surface by a-disintegrin-like and metalloproteinase with thrombospondin type 1 motifs (ADAM) 10 or ADAM17-mediated cleavage within the TIM-3 stalk region, resulting in a soluble form of TIM-3 (sTIM-3) [14], which is elevated in the sera of patients with autoimmune diseases [15].