Reply to Levis and Rendini

Reply to Levis and Rendini—We appreciate the comments by Levis et al. on our work documenting the potential utility of clofazimine for the treatment of tuberculosis. We support their view on the efficacy of clofazimine in leprosy, both as an antibacterial and an anti-inflammatory agent. In addition to mycobacterial infections, the vast majority of infectious diseases and cancers involve pathology induced by inflammation. Although inflammatory responses play a central role in inducing protective immune responses, profound inflammation can exacerbate pathology. Thus, the addition of anti-inflammatory agents to the treatment regimens for certain infections and cancers might be beneficial. Consistent with this notion, corticosteroids enhance the efficacy of tuberculosis treatment regimens [1]. However, corticosteroids also suppress host immunity, which might have deleterious effects on the host, such as the risk for disease relapse and reinfection. Clofazimine, an inhibitor of the voltage-gated K⁺ channel Kv1.3, has antimicrobial and anti-inflammatory activities and is beneficial for the treatment of infectious diseases such as leprosy [2] and tuberculosis [3]. Interestingly, effector memory T (T_EM) cells abundantly express Kv1.3. We have recently shown that inhibition of Kv1.3 by clofazimine promotes the induction of long-lived, antigen-specific central memory T (T_CM) cells, which are crucially important for the efficacy of vaccines [4]. Therefore, clofazimine may be effective as an adjunct to a variety of therapies and vaccines:

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