Endothelial cell activation and proliferation modulate NKG2D activity by regulating MICA expression and shedding.

MICA are major histocompatibility complex class I-related molecules, expressed by endothelial cells (ECs), that may be targets for alloantibodies and NKG2D-expressing natural killer (NK) and T effector cells in organ allografts. This study shows that basal levels of MICA expressed on vascular ECs is sufficient to functionally modulate the expression and activity of the immunoreceptor NKG2D in allogeneic NK cells. We found that MICA expression is differentially regulated at the EC surface in response to cytokines.

Protective cross talk between activated protein C and TNF signaling in vascular endothelial cells: implication of EPCR, noncanonical NF-κB, and ERK1/2 MAP kinases.

Activated protein C (APC) is a natural anticoagulant protease that displays cytoprotective and antiinflammatory activities and has been demonstrated to reduce mortality of patients with severe sepsis. However, APC signaling is not fully understood. This study further investigated the antiinflammatory effects of APC in vascular endothelial cells (EC) and examined the cross talk between APC and TNF signaling.

Vascular endothelial cells evade apoptosis triggered by human leukocyte antigen-DR ligation mediated by allospecific antibodies.

Background: Human leukocyte antigen (HLA)-DR ligation mediates cell death of antigen-presenting cells (APC), including mature B cells, macrophages, and dendritic cells. This study investigates the apoptotic effects of HLA class II ligation mediated by anti-HLA antibodies on activated human vascular graft endothelial cells (ECs).

Methods: HLA class II expression was examined by flow cytometry using a panel of HLA-typed vascular ECs isolated from transplant donors and compared with that of B lymphocytes.