RT Journal Article SR Electronic T1 Tuberculosis complicating imatinib treatment for chronic myeloid leukaemia JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP 670 OP 672 DO 10.1183/09031936.00025408 VO 33 IS 3 A1 Daniels, J. M. A. A1 Vonk-Noordegraaf, A. A1 Janssen, J. J. W. M. A1 Postmus, P. E. A1 van Altena, R. YR 2009 UL //www.qdcxjkg.com/content/33/3/670.abstract AB Although imatinib is not considered a predisposing factor for tuberculosis (TB), the present case report describes three patients in whom imatinib treatment for chronic myeloid leukaemia was complicated by TB. This raises the question of whether imatinib increases susceptibility to TB. There are several reports suggesting that imatinib might impair the immune system, leading to a variety of infections, including varicella zoster and hepatitis B. Control of TB in healthy individuals is achieved through acquired immunity, in which antigen-specific T-cells and macrophages arrest growth of Mycobacterium tuberculosis bacilli and maintain control over persistent bacilli. In the chronic stage of the infection, CD8+ T-cells assist macrophages in controlling intracellular mycobacteria. The T-cell receptor orchestrates this process. The fact that tyrosine kinases play an important role in T-cell receptor signal transduction and that imatinib has been shown to affect T-cell receptor signal transduction, presents a mechanism by which imatinib might impair control of Mycobacterium tuberculosis; thereby leaving the host susceptible to reactivation of tuberculosis.