DC-SIGN Is the Major Mycobacterium tuberculosis Receptor on Human Dendritic Cells

By L. Tailleux, Olivier Schwartz, J. Herrmann, Elisabeth Pivert, M. Jackson, A. Amara, L. Legrès, D. Dreher, L. Nicod, J. Gluckman and 3 more. Journal of Experimental Medicine, 2003

688 citations recorded by the source corpus.

Early interactions between lung dendritic cells (LDCs) and Mycobacterium tuberculosis, the etiological agent of tuberculosis, are thought to be critical for mounting a protective anti-mycobacterial immune response and for determining the outcome of infection. However, these interactions are poorly understood, at least at the molecular level. Here we show that M. tuberculosis enters human monocyte-derived DCs after binding to the recently identified lectin DC-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN). By contrast, complement receptor (CR)3 and mannose receptor (MR), which are the main M. tuberculosis receptors on macrophages (Mφs), appeared to play a minor role, if any, in mycobacterial binding to DCs. The mycobacteria-specific lipoglycan lipoarabinomannan (LAM) was identified as a key ligand of DC-SIGN. Freshly isolated human LDCs were found to express DC-SIGN, and M. tuberculosis–derived material was detected in CD14−HLA-DR+DC-SIGN+ cells in lymph nodes (LNs) from patients with tuberculosis. Thus, as for human immunodeficiency virus (HIV), which is captured by the same receptor, DC-SIGN–mediated entry of M. tuberculosis in DCs in vivo is likely to influence bacterial persistence and host immunity.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/1d359027d5e369465904c7109724394bb21ff629

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Citations in the corpus

HIV and Tuberculosis: a Deadly Human Syndemic (2011, result): “tuberculosis resides in macrophages has been known at least since the studies of Sabin and colleagues in the 1920s (65, 220), although the spectrum of cells in which the bacteria reside in vivo has been recently found to include myeloid dendritic cells (129, 244, 269).”
Microbial stimulation fully differentiates monocytes to DC-SIGN/CD209+ dendritic cells for immune T cell areas (2010, background): “, 2002) or in transducing inhibitory signals as seen when human DC-SIGN/CD209 interacts with mycobacteria (Geijtenbeek et al., 2003; Tailleux et al., 2003).”
Direct recognition of the mycobacterial glycolipid, trehalose dimycolate, by C-type lectin Mincle (2009, background): “Another C-type lectin receptor, DC-SIGN, is known to recognize mycobacteria (Tailleux et al., 2003), but its binding results in the down-regulation of dendritic cell–mediated immune responses (Geijtenbeek et al., 2003).”
From carbohydrate leads to glycomimetic drugs (2009, background): “In addition to HIv, various other pathogens -such as the hepatitis C virus 54 , Dengue virus 55 , Ebola virus 56 , Marburg virus 57 , coronavirus (which causes severe acute respiratory syndrome) 58 and cytomegalovirus 59 , as well as bacteria such as Mycobacterium tuberculosis 60 and Helicobacter py”
Dendritic-cell control of pathogen-driven T-cell polarization (2003, background): “71 ), Mycobacteria species that bind to DC-SIGN with their mannosylated lipoarabinomanna”