Monoclonal antibody to CD9 inhibits platelet-induced human endothelial cell proliferation.

Platelets are anucleate cytoplasmic fragments derived from bone marrow megakaryocytes, and endothelial cells constitute the barrier between bloodstream and adjacent tissues. Although platelets are thought to regulate the biological functions of endothelial cells, the molecular mechanisms involved are poorly understood. With human umbilical vein endothelial cells and freshly isolated platelets, we established an in vitro model of platelet-induced endothelial cell proliferation.

TGF-beta inhibits Fas-mediated apoptosis of a follicular dendritic cell line by down-regulating the expression of Fas and caspase-8: counteracting role of TGF-beta on TNF sensitization of Fas-mediated apoptosis.

Follicular dendritic cells (FDC) constitute the framework of germinal center (GC) in secondary lymphoid follicles, and the integrity of FDC networks is critically affected by cytokines present in the GC. We have previously shown that TNF promotes Fas-mediated apoptosis of HK cells, an established FDC-like cell line, by up-regulating Fas expression. However, in the developing GC, FDC death is not a hallmark of GC despite the presence of TNF and FasL.

Fibroblasts enhance the in vitro survival of human memory and naïve B cells by maintaining intracellular levels of glutathione.

To gain insight into the mechanism of memory B cell survival, we cultured highly purified subpopulations of tonsillar B cells with tonsillar fibroblasts. The fibroblasts greatly enhanced the survival of memory and naïve B cells but did not delay the rapid apoptosis of germinal center B cells. B cell activation was not observed during the period of culture, as shown by the absence of activation markers and of cycling cells.