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CD209 — IL10

Pathways - manually collected, often from reviews:

• KEGG Tuberculosis: CD209/CLEC4M → IL10 (protein-protein, activation)

Text-mined interactions from Literome

Koppel et al., Immunobiology 2004 : Recent studies have demonstrated that M. tuberculosis targets the DC-specific C-type lectin DC-SIGN to inhibit the immuno-stimulatory function of DC through the interaction of the mycobacterial mannosylated lipoarabinomannan ( ManLAM ) to DC-SIGN, which prevents DC maturation and induces the immuno-suppressive cytokine IL-10
Gurney et al., J Virol 2005 (HIV Infections) : Ex vivo and in vitro data implicate the role of IL-10 in upregulating DC-SIGN expression and downregulating expression of the costimulatory molecules CD80/CD86
Gagliardi et al., J Leukoc Biol 2005 : This would occur through the interaction of the mycobacterial mannosylated lipoarabinomannan to DC-SIGN , which would prevent DC maturation and induce the immunosuppressive cytokine interleukin (IL)-10 synthesis
Caparrós et al., Blood 2006 (Calcium Signaling...) : The relevance of the DC-SIGN initiated signals was demonstrated in monocyte derived dendritic cells, as DC-SIGN cross linking synergizes with TNF-alpha for IL-10 release and enhances the production of LPS induced IL-10
Wieland et al., Microbes Infect 2007 (Disease Models, Animal...) : M. tuberculosis targets dendritic cell ( DC ) -specific intercellular adhesion molecule-3 grabbing non-integrin ( DC-SIGN ) to induce immunosuppression, since interaction of DC-SIGN with mycobacterial mannose capped lipoarabinomannan ( ManLAM ) induces interleukin (IL)-10 and prevents DC maturation
Geurtsen et al., J Immunol 2009 : As for mannose capped lipoarabinomannan, an abundant mycobacterial cell wall associated glycolipid, binding of alpha-glucan to DC-SIGN stimulated the production of immunosuppressive IL-10 by LPS activated monocyte derived dendritic cells
van Vliet et al., PLoS Pathog 2009 : Whereas N. gonorrhoeae variant A with a terminal N-acetylglucosamine on its LOS was recognized by DC-SIGN and induced significantly more IL-10 production, phenotype C, carrying a terminal N-acetylgalactosamine, primarily interacted with MGL and skewed immunity towards the T helper 2 lineage