Extended Data Fig. 2: IgA targets Candida species but not S. cerevisiae.
From: Adaptive immunity induces mutualism between commensal eukaryotes
a, IgA-bound faecal fungi gating strategy. b, Peyer’s patch GC B cell and TFH cell gating strategy. c, Colon LP IgA plasma cell gating strategy (n = 4 mice per group 30 days after inoculation; representative of two experiments for b, c). d, IgA binding to faecal GFP+ S. cerevisiae and GFP+ C. albicans in monocolonized SW mice. e, Total IgA levels from monocolonized SW mice. f, Flow cytometry quantification of SW IgA binding to cultured S. cerevisiae and C. albicans (n = 4 C. albicans-colonized and n = 5 S. cerevisiae-colonized, one experiment for d–f). g, h, Serum antibody binding to cultured C. albicans or S. cerevisiae from SW (g) or B6 (h) GF or monocolonized mice. Antibody quantified by flow cytometry from serum diluted 1:25 (SW: GF n = 4, Sc-colonized n = 5, Ca-colonized n = 5; B6: GF n = 3, Sc n = 5, Ca-colonized n = 3). i, Lumen and tissue-associated fungal burden in monocolonized B6 mice 30 days after inoculation (n = 4 mice per group; one experiment; representative of two experiments). j, Whole-intestinal IgA four weeks after inoculation. k, Caecal wash IgA binding to cultured C. glabrata measured by flow cytometry. l, Peyer’s patch TFH cells four weeks after inoculation. m, Peyer’s patch GC B cells (n = 4 mice per group; one experiment for j–m). n, IgA binding to cultured C. glabrata, S. cerevisiae and C. albicans from faecal wash from GF, C. albicans-monocolonized or C. glabrata-monocolonized intestinal wash (n = 2 C. albicans, n = 3 C. glabrata and n = 3 S. cerevisiae faecal washes) o, Percentage of IgA binding and binding intensity of faecal C. albicans during colonization of antibiotic-treated wild-type and Tcrb−/− mice (n = 6 Tcrb−/− and n =8 wild-type mice from two experiments). P values calculated using two-way ANOVA (d, o), with Sidak’s test (b, e, f, g, h, n), or two-sided unpaired t-test (j, k, l, m). Mean values ± s.d. for b, d–o.
