Extended Data Fig. 2. IgA coating of tumour cells is associated with a better outcome in HGSOC.

a, Bar graphs representing tumour-wise FACS analysis (n = 10) comparison of percentages of each Ig⁺ cells among total Ig⁺ plasmablasts (intracellular in CD45⁺CD3⁻CD19⁺CD20⁻CD38^high) and CD27⁺ plasmablasts (intracellular in CD45⁺CD3⁻CD19⁺CD20⁻CD38^highCD27⁺), normalized to 10,000 viable CD45⁺ cells. b, Relative abundances of IgH chains on the basis of TCGA transcriptional analyses (n = 430) for each immunoglobulin heavy chain gene. Abundances are shown in log₂-transformed reads per kilobase of transcripts (RPKM) values, which corrects for both gene length and sequencing depth. Details of box plots are in Methods. c, Overall survival associated with the presence of CD19⁺CD138⁺ plasma cells within the total tumour area (P = 0.0285) (left) or specifically in the PCK⁺ epithelial tumour islets (P = 0.0053) (right), in HGSOC as assessed by multiplex immunohistochemistry of TMAs corresponding to 534 patients with HGSOC combined from the NECC (n = 180), NHS (n = 261) and MCC (n = 93). Plasma cell infiltration is defined as the presence of CD19⁺CD138⁺ cells on any of the duplicate sections analysed for each tumour. *P ≤ 0.05, **P ≤ 0.01, two-sided log-rank (Mantel–Cox) test. d, FACS analysis showing number (log-transformed) of plasma cells (CD45⁺CD3⁻CD19⁺CD20⁻CD138⁺ and CD45⁺CD3⁻CD19⁻CD20⁻CD138⁺), plasmablasts (CD45⁺CD3⁻CD19⁺CD20⁻CD38^high), B cells (CD45⁺CD3⁻CD19⁺CD20⁺), T cells (CD45⁺CD3⁺) and other leukocytes (CD45⁺CD3⁻CD19⁻CD20⁻CD138⁻) in HGSOC (n = 29). The data are normalized to 10,000 viable CD45⁺ leukocytes. Data are mean ± s.e.m. e, Graphs showing correlations between log count of T cells and plasma cells (left) (Pearson correlation coefficient (r) = 0.5049; two-sided nominal P = 0.0052); and between log count of T cells and plasmablasts (right) (Pearson correlation coefficient (r) = 0.4755; two-sided nominal P = 0.0091). All three cell types represent absolute counts normalized to 10,000 CD45⁺ leukocytes. f, Colocalization of IgA with pIgR⁺ cells (IgA–pIgR co-localization ≥ median) in the PCK⁺ tumour islets is associated with an improved outcome in HGSOC, compared to only pIgR^high samples (≥median) without IgA colocalization (colocalization < median), in MCC (P = 0.0060) and NECC (P = 0.0044) cohorts. **P ≤ 0.01, two-sided log-rank (Mantel–Cox) test. g, Higher number of IgA-coated cells in the PCK⁻ stromal area (average from duplicated cores) is not associated with an improved outcome in HGSOC, analysed using median IgA-coating threshold in MCC (P = 0.8954) and NECC (P = 0.0537) cohorts. NS, not significant; two-sided log-rank (Mantel–Cox) test, no multiple comparison adjustment. h, A higher number of IgG-coated cells in the PCK⁺ tumour islets (average from duplicated cores) is not associated with an improved outcome in HGSOC, analysed using median IgG-coating threshold in MCC (P = 0.6350) and NECC (P = 0.0731) cohorts. NS, not significant; two-sided log-rank (Mantel–Cox) test.

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