The cell surface phenotype of human dendritic cells.

Dendritic cells (DC) are bone marrow derived leucocytes that are part of the mononuclear phagocytic system. These are surveillance cells found in all tissues and, as specialised antigen presenting cells, direct immune responses. Membrane molecules on the DC surface form a landscape that defines them as leucocytes and part of the mononuclear phagocytic system, interacts with their environment and directs interactions with other cells. This review describes the DC surface landscape, reflects on the different molecules confirmed to be on their surface and how they provide the basis for manipulation and translation of the potent functions of these cells into new diagnostics and immune therapies for the clinic.

Hemolytic disease of the fetus and newborn caused by anti-Hr0 in a 27-year-old female with Dc- phenotype: A case report.

Anti-Hr0 (Anti-Rh17) is a rare immune Immunoglobulin G (IgG) to high-frequency Rh antigens that may cause severe and often fatal Hemolytic disease of the fetus and newborn (HDFN) in D--, Dc- and DCw- mothers who have been exposed to red cells of the common Rh phenotype by transfusion or pregnancy. Several pregnant women have been affected by this antibody leading to perinatal death. Therefore, immediate and effective management of these cases is of great importance. We report a case of HDFN in a 27-year-old (G5, P3, L1), woman with Rh Dc- phenotype managed successfully using intravenous immunoglobulin (IVIg) and simple transfusions.

Cholecalciferol modulates the phenotype of differentiated monocyte-derived dendritic cells without altering HIV-1 transfer to CD4+ T cells.

Background Dendritic cells (DCs) play a crucial role during HIV-1 transmission due to their ability to transfer virions to susceptible CD4+ T cells, particularly in the lymph nodes during antigen presentation which favors the establishment of systemic infection. As mature dendritic cells (mDCs) exhibit a greater ability to transfer virions, compared to immature DCs (iDCs), maintenance of an iDC phenotype could decrease viral transmission. The immunomodulatory vitamin D (VitD) has been shown to reduce activation and maturation of DCs; hence, we hypothesized that it would reduce viral transference by DCs. Materials and methods We evaluated the effect of in vitro treatment with a precursor of VitD, cholecalciferol, on the activation/maturation phenotype of differentiated monocyte-derived DCs and their ability to transfer HIV-1 to autologous CD4+ T cells. Results Our findings show that although cholecalciferol decreases the activation of iDCs, it did not impact the maturation phenotype after LPS treatment nor iDCs' ability to transfer viral particles to target cells. Conclusion These findings suggest that despite cholecalciferol potentially modulates the phenotype of mucosal iDCs in vivo, such modulation might not impact the ability of these cells to transfer HIV-1 to target CD4+ T cells.