PT - JOURNAL ARTICLE AU - J. M. A. Daniels AU - A. Vonk-Noordegraaf AU - J. J. W. M. Janssen AU - P. E. Postmus AU - R. van Altena TI - Tuberculosis complicating imatinib treatment for chronic myeloid leukaemia AID - 10.1183/09031936.00025408 DP - 2009 Mar 01 TA - European Respiratory Journal PG - 670--672 VI - 33 IP - 3 4099 - http://erj.ersjournals.com/content/33/3/670.short 4100 - http://erj.ersjournals.com/content/33/3/670.full SO - Eur Respir J2009 Mar 01; 33 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.