Extended Data Fig. 2: MrgprA3 neurons promote cutaneous inflammation and host immunity against S. mansoni.
(a), Representative counterplots and quantification of skin macrophages by flow cytometry of wildtype (WT) mice treated with vehicle or chloroquine (CQ). Mean ± s.e.m (n = 4). (b), Ear thickness measured daily during photostimulation of ChR2 control or MrgprA3-ChR2 mice. Mean ± s.e.m (n = 3-4). (c,d), Proportions and absolute cell numbers of skin IL-17+ αβ T cells, IL-17+ ILCs, and Foxp3+ Tregs were quantified by flow cytometry of control or MrgprA3-ChR2 mice 5 days post-optogenetic stimulation. Mean ± s.e.m (n = 6-7). (e), Ear thickness was measured daily during vehicle or CQ treatment of WT mice. Mean ± s.e.m (n = 4). (f), FFPE ear skin sections from mice treated with vehicle or CQ were analyzed by H&E staining and (g), Epidermal thickness was quantified. Mean ± s.e.m (n = 4-5). (h), Representative counterplots and quantification of skin IL-17+ γδ T cells by flow cytometry of WT mice treated with vehicle or CQ. Mean ± s.e.m (n = 4). (i), Ear thickness was measured every 3-4 days of control or MrgprA3-DTR mice treated with diphtheria toxin (DT) administered every 3 days for 3 weeks. Mean ± s.e.m (n = 4-5). (j-l), One day after S. mansoni challenge, neutrophil (CD11b+ Ly6G+ Ly6Cint) ear skin responses were evaluated in ChR2 control or MrgprA3-ChR2 mice; vehicle or CQ-treated mice; and DTR control or MrgprA3-DTR mice. Mean ± s.e.m (n = 4-5). P values were determined by two-tailed Student’s t-tests or Two-way ANOVA with post hoc correction. *P<0.05, **P<0.01, ***P<0.001. Representative of 2-3 independent experiments, each with ≥4 biological replicates.
