Figure 2
Figure 2. Experimental filtration mitigates the priming activity of human antibodies against HLA-A2 and HNA-3a. (A) Priming of the fMLF-activated, superoxide dismutase inhibitable respiratory burst (nmol O2−/min) in PMNs from HLA-A2 homozygotes primed with FP, unmodified plasma with antibodies to HLA-A2, and filtered plasma with antibodies to HLA-A2. Experimental filtration mitigated the priming activity, which was not different from the FP-treated controls. (B) Priming of the fMLF-activated, superoxide dismutase inhibitable respiratory burst in HNA-3a+ PMNs primed with FP, unmodified plasma that contains antibodies to HNA-3a, and experimentally filtered plasma that contains antibodies to HNA-3a. Experimental filtration mitigated the HNA-3a priming activity. *P < .05 vs all groups, n = 5.

Experimental filtration mitigates the priming activity of human antibodies against HLA-A2 and HNA-3a. (A) Priming of the fMLF-activated, superoxide dismutase inhibitable respiratory burst (nmol O2/min) in PMNs from HLA-A2 homozygotes primed with FP, unmodified plasma with antibodies to HLA-A2, and filtered plasma with antibodies to HLA-A2. Experimental filtration mitigated the priming activity, which was not different from the FP-treated controls. (B) Priming of the fMLF-activated, superoxide dismutase inhibitable respiratory burst in HNA-3a+ PMNs primed with FP, unmodified plasma that contains antibodies to HNA-3a, and experimentally filtered plasma that contains antibodies to HNA-3a. Experimental filtration mitigated the HNA-3a priming activity. *P < .05 vs all groups, n = 5.

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