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Mycobacterium tuberculosis is the causal agent of tuberculosis. Tumor necrosis factor alpha (TNF-␣), transforming growth factor ␤ (TGF-␤), and gamma interferon (IFN-␥) secreted by activated macrophages and lymphocytes are considered essential to contain Mycobacterium tuberculosis infection. The CD43 sialomucin has been reported to act as a receptor for bacilli through its interaction with the chaperonin Cpn60.2, facilitating mycobacterium-macrophage contact. We report here that Cpn60.2 induces both human THP-1 cells and mouse-derived bone marrow-derived macrophages (BMMs) to produce TNF-␣ and that this production is CD43 dependent. In addition, we present evidence that the signaling pathway leading to TNF-␣ production upon interaction with Cpn60.2 requires active Src family kinases, phospholipase C-␥ (PLC-␥), phosphatidylinositol 3-kinase (PI3K), p38, and Jun N-terminal protein kinase (JNK), both in BMMs and in THP-1 cells. Our data highlight the role of CD43 and Cpn60.2 in TNF-␣ production and underscore an important role for CD43 in the host-mycobacterium interaction.

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