Retinoic Acid Imprints a Mucosal-like Phenotype on Dendritic Cells with an Increased Ability To Fuel HIV-1 Infection

摘要: The tissue microenvironment shapes the characteristics and functions of dendritic cells (DCs), which are important players in HIV infection dissemination. Notably, DCs gut have daunting task orchestrating balance between immune response tolerance. They produce retinoic acid (RA), imprints a gut-homing phenotype influences surrounding DCs. To investigate how impacts ability to drive infection, we conditioned human immature monocyte-derived (moDCs) with RA (RA-DCs), before pulsing them mixing autologous T cells. RA-DCs showed semimature, mucosal-like released higher amounts TGF-β1 CCL2. Using flow cytometry, Western blot, microscopy, determined that moDCs express cell adhesion molecule mucosal vascular addressin molecule-1 (MAdCAM-1) increases its expression. MAdCAM-1 was also detected on small population rhesus macaque ( Macaca mulata ) mesenteric lymph node. formed more DC–T conjugates promoted significantly replication mixtures compared moDCs. This correlated increase Blocking partially inhibited enhanced replication. In summary, DC phenotype, increasing their exacerbate infection. We describe previously unknown mechanism may contribute rapid spread gut, major site after exposure.