Aims: Clinically significant antibodies may become undetectable and still provoke transfusion reactions. Hemolysis has been reported among transfusion recipients with anti-Kidd that was undetectable by gel column but detectable by other methods.
Methods: We compared two automated technologies - microplate (MP) and gel column (GC) methods - with manual methods in ABO/RhD typing, irregular antibody screening, identification, titration, and detection threshold of mixed-field agglutination. Results: Automated systems agreed generally with tube results in 98% or more of ABO forward and RhD groupings, but showed weaker reactions in ABO reverse testing against A1 (K=0.88 with MP and K=0.77 with GC) and B cells (K=0.66 with MP and K=0.68 with GC) and failed to detect some anti-A (2 of 273 samples with MP) and anti-B (2 of 273 with MP and 1 of 272 with GC). MP missed 2 (anti-E and –Fyb) of 8 antibodies and GC missed 5 (2 anti-E and 1 each of -Fyb, -Jka and –Lea) of 10 antibodies, which manual PEG-IAT detected. Among 11 known alloantibodies, MP detected 7 antibodies at higher dilution than tube PEG-IAT, whereas GC showed lower scores in 7 samples than tube PEG-IAT and missed 2 clinically significant antibodies (anti-C and anti-Fyb).
Conclusion: Automated systems, comparable to manual tube technique for forward grouping of ABO and RhD, are less sensitive in ABO reverse testing. As GC more often failed to detect clinically significant antibodies of low-titer, users should be especially mindful of possible post-transfusion hemolysis.
Ikarugamycin (IK) is an antibiotic which has been reported to have a variety of functions, such as inhibition of clathrin-mediated endocytosis (CME), anti-tumor effects and regulation of the immune system. Whether IK influences cytokine production is poorly understood. We have investigated the relationship between IK and production of tumor necrosis factor-α (TNF). TNF plays a pivotal role in pathogenesis of many diseases. Although the dynamics of soluble TNF (sTNF) has been widely explored so far, the functions of the membrane form of TNF (mTNF) have not been fully elucidated. We demonstrated that IK increases the amount of mTNF and prolongs the duration of TNF expression. This effect is unrelated to the shedding activity of disintegrin and metalloproteinase domain-containing protein 17 (ADAM 17). Our results revealed that there is a mechanism to terminate inflammation at the cellular level which IK dysregulates. Furthermore, IK can be a tool to study TNF signaling due to its effect of increasing mTNF expression.
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