Immunobiologic consequences of assist devices.

The aberrant state of monocyte and T-cell activation resulting from these host-device interaction is accompanied by two parallel processes: (1) selective loss of Th1 cytokine-producing CD4 T cells through activation-induced cell death, and (2) unopposed activation of Th2 cytokine-producing CD4 T cells resulting in B-cell hyperreactivity and dysregulated immunoglobulin synthesis via Th2 cytokines and heightened CD40 ligand-CD40 interactions. The net result of these events is that on one hand the VAD recipient develops progressive defects in cellular immunity and is at increased risk of serious infection, and on the other hand the VAD recipient is more likely to develop allosensitization, posing a significant risk to successful transplant outcome.