Allogeneic Ex Vivo Expanded Corneal Epithelial Stem Cell Transplantation: A Randomized Controlled Clinical Trial.

Limbal stem cell deficiency (LSCD) is a disease resulting from the loss or dysfunction of epithelial stem cells, which seriously impairs sight. Autologous limbal stem cell transplantation is effective in unilateral or partial bilateral disease but not applicable in total bilateral disease. An allogeneic source of transplantable cells for use in total bilateral disease can be obtained from culture of donated cadaveric corneal tissue.

Dendritic cells previously exposed to mannan-binding lectin enhance cytokine production in allogeneic mononuclear cell cultures.

Mannan (or mannose)-binding lectin (MBL) can bind to monocytes and dendritic cells, but the significance of such interactions is unknown. We hypothesized that the presence of MBL might prevent the differentiation of monocytes into monocyte-derived dendritic cells or interfere with the development of dendritic cells in some way. We therefore investigated the influence of recombinant human MBL on surface antigen expression and on secretion of selected cytokines.

Is mannan-binding lectin (MBL) detectable on monocytes and monocyte-derived immature dendritic cells?

MBL (mannan-binding lectin; also called mannose-binding lectin) is a circulating C-type lectin with a collagen-like region synthesized mainly by the liver. MBL may influence susceptibility to infection in recipients of stem cell transplants, and it has even been suggested that the MBL status of a donor can influence the recipient's susceptibility to post-transplant infections. We have previously reported that MBL can be detected on human monocytes and monocyte-derived dendritic cells, based on detection using biotinylated anti-MBL, suggesting that those cells could synthesize MBL.

Immature dendritic cells possess a sugar-sensitive receptor for human mannan-binding lectin.

Mannan-binding lectin (MBL) is a collectin synthesized by the liver and secreted into the bloodstream. It has a receptor for microbial structures in its C-type lectin domain and a separate receptor(s) located within its collagen-like region for autologous phagocytic cells. Here we demonstrate that human peripheral blood adherent cells (monocytes) and monocyte-derived dendritic cells are a source of MBL, and that a novel calcium-dependent and sugar-specific MBL receptor is up-regulated in immature (CD1a-positive) dendritic cells.