Notch2 is not robustly expressed by cecum basophils in T. muris-infected AKR/J mice.
Previous findings from our group reported a key role for Notch signaling in programming helminth-induced basophil responses in C57BL/6 mice, associated Type 2 inflammation and helminth expulsion, but not basophil population expansion (7). Therefore, we sought to determine whether Notch2, the predominant Notch receptor expressed on C57BL/6 basophils during infection (7), was expressed on the surface of AKR/J basophils. Overall, there was no significant infection-induced increase in the percentage of basophils that expressed Notch2 (Fig. 3A-B) or in the Notch2 gMFI of Notch2 positive basophils (Fig. 3C) in the cecum following T. muris infection. In the spleen, the percentage of basophils that expressed Notch2 at d19 p.i. increased slightly over levels observed in naïve mice, but then declined (Fig. S2A-B), and there were no infection-induced changes in the Notch2 gMFI of Notch2-positive splenic basophils (Fig. S2C). Thus, these data suggest that while susceptible AKR/J mice do have expanded basophil populations afterT. muris infection, these basophils do not display a substantial infection-induced increase in the level of surface Notch2 expression.