Frequency and specificity of the Trima Accel "verify WBCs" advisory: considerations for product management.

BACKGROUND: The Trima Accel displays a "verify WBCs" message if the plateletpheresis product (PLT) may not be leukoreduced (LR). Most blood banks require sensitive white blood cell (WBC) testing of these PLTs by flow or Nageotte. We evaluated how often these PLTs were non-LR by European or US Food and Drug Administration (FDA) criteria and whether sensitive WBC testing is necessary. STUDY DESIGN AND METHODS: Phase 1 reviewed the frequency of this message with various procedure types and the flow WBC results for PLTs with or without the message. Phase 2 assessed how many FDA LR failures were detectable by a hematology analyzer. In Phase 3, PLTs were managed by hematology analyzer results. RESULTS: In Phase 1, 3.8% of PLT-only and 11.1% of PLT-plasma collections had the "verify WBCs" message. Only 1% of "verify" PLTs contained more than 1 × 10(6) WBCs and only 0.5% were FDA LR failures. In Phase 2, 10 of 670 "verify" PLTs and one nonflagged PLT were FDA LR failures. Six of 11 LR failures had hematology analyzer WBC concentrations of 0.4 × 10(9) /L or higher. In Phase 3, "verify" PLTs were allowed in inventory if hematology analyzer WBC concentration was below 0.4 × 10(9) /L; inventory quality control showed no FDA LR failures by flow. Trima Version 6.0 software lowered the "verify" message frequency in PLT-plasma procedures but not in PLT-only procedures. CONCLUSION: Four percent of Trima PLT collections have the "verify WBCs" message but almost all of these are LR by European and FDA criteria. Fifty percent of FDA LR failures were detectable by a hematology analyzer. Sensitive WBC testing of all "verify WBCs" PLTs may not be necessary to satisfy LR quality assurance requirements.

T(H)1, T(H)2, and T(H)17 cells instruct monocytes to differentiate into specialized dendritic cell subsets.

Monocytes and T helper (T(H)) cells rapidly infiltrate inflamed tissues where monocytes differentiate into inflammatory dendritic cells (DCs) through undefined mechanisms. Our studies indicate that T(H) cells frequently interact with monocytes in inflamed skin and elicit the differentiation of specialized DC subsets characteristic of these lesions. In psoriasis lesions, T(H)1 and T(H)17 cells interact with monocytes and instruct these cells to differentiate into T(H)1- and T(H)17-promoting DCs, respectively. Correspondingly, in acute atopic dermatitis, T(H)2 cells interact with monocytes and elicit the formation of T(H)2-promoting DCs. DC formation requires GM-CSF and cell contact, whereas T(H) subset specific cytokines dictate DC function and the expression of DC subset specific surface molecules. Moreover, the phenotypes of T cell-induced DC subsets are maintained after subsequent stimulation with a panel of TLR agonists, suggesting that T(H)-derived signals outweigh downstream TLR signals in their influence on DC function. These findings indicate that T(H) cells govern the formation and function of specialized DC subsets.