부산대학교 도서관

An estimated one-third of the world's population is infected with Mycobacterium tuberculosis, although most affected individuals maintain a latent infection. This control is attributed to the formation of granulomas, cell masses largely comprising infected macrophages with T cells aggregated around them. Inflammatory DCs, characterized as CD11[c.sup.+]CD11[b.sup.+]Ly6[C.sup.+], are also found in granulomas and are an essential component of the acute immune response to mycobacteria. However, their function during chronic infection is less well understood. Here, we report that [CD11c.sup.+] cells dynamically traffic in and out of both acute and chronic granulomas induced by Mycobacterium bovis strain bacillus Calmette-Guerin (BCG) in mice. By transplanting Mycobacterium-induced granulomas containing fluorescently labeled [CD11c.sup.+] cells and bacteria into unlabeled mice, we were able to follow [CD11c.sup.+] cell trafficking and T cell activation. We found that half of the [CD11c.sup.+] cells in chronic granulomas were exchanged within 1 week. Compared with tissue-resident DC populations, [CD11c.sup.+] cells migrating out of granulomacontaining tissue had an unexpected systemic dissemination pattern. Despite low antigen availability, systemic [CD4.sup.+] T cell priming still occurred during chronic infection. These data demonstrate that surveillance of granulomatous tissue by [CD11c.sup.+] cells is continuous and that these cells are distinct from tissue-resident DC populations and support T cell priming during both stages of Mycobacterium infection. This intense DC surveillance may also be a feature of Mycobacterium tuberculosis infection and other granuloma-associated diseases.
Introduction The initiation and maintenance of an adequate cellular immune response have enabled an estimated 2 billion people worldwide to control, but rarely eliminate, infection with Mycobacterium tuberculosis (1). This [...]