CD8A and arthritic joint disease: Notably, a mutant IL-15 construct with impaired ability to bind IL-2Rβ (NANTIL-15) selectively blocked IL-15 signaling via the trimeric IL-15Rα/IL-2Rβ/γc receptor and reduced inflammation in a collagen-induced arthritis model, without inhibiting NK or CD8+ T cell homeostasis (70).