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To the Editor-Tuberculosis due to Mycobacterium tuberculosis is 1 of the 3 major killers among infectious diseases. Deciphering the interactions between M. tuberculosis and the innate and adaptive immune compartments of the host is critical for understanding the pathogenesis of tuberculosis and for designing effective immunotherapeutic interventions. By use of a juvenile rhesus monkey model, Qiu et al recently demonstrated that severe tuberculosis induces unbalanced up-regulation of the immune gene networks of inflammatory cytokines, chemokines, and their receptors, but low levels of T cell responses specific to purified protein derivative [1]. The authors conclude that the overexpression of immune genes after tuberculosis infection favors inflammation and suppression of antigen-specific T cells.

B Lymphocytes from Patients with Tuberculosis Exhibit Hampered Antigen‐Specific Responses with Concomitant Overexpression of Interleukin‐8