Collaboration study with Dr. Chen, who discovered increases of BST-1/CD157 in the sera and lung granuloma of the patients with tuberculosis, revealed increased susceptibility to Mycobacterium (M.) tuberculosis in Bst1-knockout mice(Bst1KO), and impaired signal transduction from TLR2/PKC zeta to production of reactive oxygen spices by macrophages lacking BST-1. In the early phase of arthritis in gp130F759, a murine model for rheumatoid arthritis, CX3CR1+ macrophage-like synoviocytes increased in the synovium and a CX3CR1+ monocyte subset decreased in the peripheral blood, indicating that local inflammation is reflected in the changes of subsets in peripheral blood. Lack of BST-1 ameliorated fibrosis in the synovium of gp130F759. We clarified physiological roles for BST-1 on macrophages in defense against M. tuberculosis and pathological roles of BST-1 promoting fibrosis in arthritis like rheumatoid arthritis.
