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Publication : Enhanced dendritic cell-induced immune responses mediated by the novel C-type lectin receptor mDCAR1.

First Author  Kaden SA Year  2009
Journal  J Immunol Volume  183
Issue  8 Pages  5069-78
PubMed ID  19786536 Mgi Jnum  J:153802
Mgi Id  MGI:4366359 Doi  10.4049/jimmunol.0900908
Citation  Kaden SA, et al. (2009) Enhanced dendritic cell-induced immune responses mediated by the novel C-type lectin receptor mDCAR1. J Immunol 183(8):5069-78
abstractText  The dendritic cell (DC) immunoreceptors (DCIR) and DC-immunoactivating receptors (DCAR) represent a subfamily of cell surface C-type lectin receptors (CLR), whose multifunctional capacities range from classical Ag uptake and immunoregulatory mechanisms to the involvement in DC ontogeny. On the basis of the generation of specific mAbs, we functionally characterized mouse DCAR1 (mDCAR1) as a member of the DCIR/DCAR family. Expression of mDCAR1 was strongly tissue dependent. mDCAR1 expression on DCs was restricted to the CD8(+) DC subset in spleen and thymus and on subpopulations of CD11b(+) myeloid cells in bone marrow and spleen, whereas the molecule was not detectable on both cell types in lymph nodes and peripheral blood. With respect to the function of CLRs as pattern recognition receptors, Ag delivered via mDCAR1 was internalized, was trafficked to early and late endosomes/lysosomes and, as a consequence, induced cellular and humoral responses in vivo even in the absence of CD40 stimulation. Intriguingly, upon triggering mDCAR1, CD8(+) DCs increased the secretion of bioactive IL-12, whereas IL-10 release is markedly reduced, thereby indicating that Ag recognized by mDCAR1 induces enhanced proinflammatory responses. These data indicate that mDCAR1 is a functional receptor on cells of the immune system and provides further insights into the regulation of immune responses by CLRs.
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