Dendritic Cells

Activation of influenza virus-specific CD4+ and CD8+ T cells: a new role for plasmacytoid dendritic cells in adaptive immunity. Fontaneau, J. F et al. Blood 2 January 2003 (DOI: 10.1182/blood-2002-10-3063)

Plasmacytoid dendritic cells (pDCs) contribute to innate immune responses to viral infections by producing type I interferons, but their ability to process and present antigens to T cells has not been demonstrated. In this study, Nina Bhardwaj's lab assessed the ability of pDCs to activate influenza-specific T cells. The results show that pDCs can process and present antigens from influenza virus to CD4+ and CD8+ T cells, and they provide the first direct evidence that pDCs contribute to the adaptive immune response to this virus. Whether such responses are protective at the level of T cells during chronic viral infection remains to be determined.

Development

Regulation of blood and lymphatic vascular separation by signaling proteins SLP-76 and Syk. Abtahian, F. et al. Science 299, 247–251 (2003)

Lymphatic vessels are derived from pre-existing blood vessels, but it is not clear which factors control the separation of emerging lymphatics from blood vessels. Mice lacking SLP76 or Syk show a failure to separate these vessels, resulting in embryonic haemorrhage and arteriovenous shunting. The transfer of bone-marrow cells derived from SLP76- or Syk-deficient animals was sufficient to recreate the abnormal vascular phenotype, which indicates that haematopoietic cells and not lymphatic endothelial cells are responsible for the defect. Further work is necessary to determine how defects in circulating cells can influence the growth of lymphatic vessels.

Infectious Disease

Mycobacteria target DC-SIGN to suppress dendritic-cell function. Geijtenbeek, T. B. H. et al. J. Exp. Med. 197, 7–17 (2003)

DC-SIGN is the major Mycobacterium tuberculosis receptor on human dendritic cells. Tailleux, L. et al. J. Exp. Med. 197, 121–127 (2003)

Although macrophages are the main cellular target of Mycobacterium tuberculosis, dendritic cells (DCs) are important mediators of immune responses against M. tuberculosis. These studies show that M. tuberculosis infects DCs using the C-type lectin receptor DC-SIGN. This interaction prevents the maturation of DCs induced by mycobacteria or lipopolysaccharide through Toll-like receptors. Interaction of mycobacteria with DC-SIGN also results in production of the anti-inflammatory cytokine IL-10, which can modify the immune response, and might promote survival of mycobacteria. These results indicate that M. tuberculosis infects DCs and interferes with DC-mediated immune responses by targeting DC-SIGN. So, DC-SIGN is a Trojan horse for M. tuberculosis as has been shown previously for HIV-1.