HLA-DR antibodies, detected in this case, had biologic functions to induce production of not only inflammatory cytokines but also neutrophil-attractant chemokines in vitro, which could contribute to the etiology of severe nonhemolytic transfusion reactions.

Both TNF-alpha and IL-1 beta, generated from PBMNCs by anti-HLA-DR plasma in a corresponding antigen-antibody-dependent manner, led to an increase in endothelial permeability. The activation of monocytes by the HLA-DR antibodies and the resultant inflammatory mediators could contribute to the pathogenesis of rash, urticaria, angioedema, and pulmonary edema after transfusion.

This method makes it possible to obtain more than 1 x 10(7) HCMV-specific T cells from approximately 2 x 10(7) to 5 x 10(7) PBMNCs without exogenous APCs such as cultured dendritic cells.