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. 2020 Sep 25;11:584254. doi: 10.3389/fimmu.2020.584254

FIGURE 1.

FIGURE 1

Pristane induces anti-KEL alloantibodies. Recipient WT mice were transfused with K1 RBCs. (A,B) Serum anti-KEL IgM and IgG in untreated mice and mice treated with pristane 2, 14, or 48 days prior to transfusion, measured by flow cytometric crossmatch. The adjusted MFI was calculated by subtracting the MFI of serum incubated with WT RBCs from the MFI of serum incubated with K1 RBCs, shown in (C). (C) Representative histograms of flow cytometric crossmatch, in which post-transfusion serum was incubated with K1 or WT RBCs. (D) Anti-KEL IgG subtypes in mice treated with or without pristane 14 days prior to transfusion. (A–D) Anti-KEL IgM was measured 4–5 days after transfusion. Anti-KEL IgG and subtypes represent the peak IgG response 21–28 days after transfusion. (E) WT mice treated with or without pristane 14 days prior to transfusion were re-transfused with a 2:1 mixture of labeled K1 and WT RBCs 35 days after the first transfusion. Control K1 recipients are negative controls. Ratios of recovered K1 and WT RBCs are calculated as percent of K1 RBCs remaining 1, 2, and 4 days after transfusion. (A–E) Representative of 3 independent experiments, 5–10 mice per group. *p < 0.05, **p < 0.01, ***p < 0.001 by Mann-Whitney U test (D) or Kruskal-Wallis test with a Dunn’s post-test (A,B,E).