Low-dose aspirin causes a significant reduction in B cells in humans. (A-B) Healthy human volunteers (n = 8) were administered with 100 mg/day of aspirin for 10 days. PB was collected before and at the end of the aspirin regime. The levels of total B cells (CD19⁺IgD⁺CD38⁻) were evaluated by flow cytometric analysis. (A) Representative results from 1 individual, as well as (B) (left) frequencies and (right) absolute cell counts of B cells in all participants were shown. (C) (Left) Representative results of p-STAT5 level in human B cells before and after taking aspirin. (Center) MFI from 3 individuals. (Right) mRNA expression of STAT5 target genes in B cells by qRT-PCR (n = 3). (D) Human peripheral blood mononuclear cells were stimulated with arachidonic acid (1 μM), human IL-7 (10 ng/mL), or both; the level of pSTAT5 in B cells was evaluated by flow cytometry analysis. (Left) Results are representative of 3 independent experiments. (Right) Expression of STAT5 target genes in sorted B cells was determined by qRT-PCR; data are mean ± SEM from 3 independent experiments (right). *P < .05 and **P < .01, using paired Student t tests and 1-way ANOVA. (E) A model for the role of COX-1 in early B-cell development: during the transition from pro-B to pre-B stage in early B-cell development, COX-1–derived TxA₂ could activate the JAK/STAT5 pathway through eliciting cAMP-PKA signaling, on binding with TP, which leads to the transcription of STAT5 target genes, including Pax5, and eventually promotes B-cell development.