[Immunity against mycobacterium tuberculosis and risk of biological anti-rheumatic agents]

A third of world's population is invaded with Mycobacterium tuberculosis, about 9.0 million people developed tuberculosis (TB) illness and 1.3 million people died from the disease every year. Acquired immunity (cytotoxic CD8(+) T cell, Th1 CD4(+) helper T cell) and macrophage play important role for TB infection. Recently, natural immunity also play a very attractive role for the development TB immunity, with several cytokines, microbicidal proteins and Toll-like receptors. The introduction and uptake of biological disease-modifying anti-rheumatic drugs has dramatically advanced and improved the standard care and the prognosis of patients with rheumatoid arthritis (RA). However, as clinical experience with these drugs has grown, risk of granulomatous infections - especially disseminated tuberculosis in adult RA - and reactivation of hepatitis B virus (HBV) are focused. This year marks the tenth anniversary of the approvals of the first tumor necrosis factor (TNF)-alpha antagonist for the treatment of rheumatoid arthritis in Japan. Our understanding of this subject and the knowledge of basic immunology has also advanced during ten years. This review especially focuses on the pathologic action of the TNF blockers in the development of secondary (disseminated) tuberculosis.