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. Author manuscript; available in PMC: 2026 Oct 25.
Published in final edited form as: Cell Rep. 2026 Sep 9;45(9):117969. doi: 10.1016/j.celrep.2026.117969

Figure 3. Cytokine-producing B cells contribute to ICI-colitis by supporting proinflammatory T cells.

Figure 3.

(A) Percent of colonic B cells expressing IL-17A and IL-6, and plasma cells expressing IgG1 and IgA from healthy mice and DSS-primed mice with or without combo ICIs (n = 5 per group).

(B) Percent of mLN B cells expressing IL-17A and IL-6, and plasma cells expressing IgG1 and IgA from healthy mice and DSS-primed mice with or without combo ICIs (n = 5 per group).

(C) Experimental scheme. Blocking mAbs targeting CD19, B220, and CD22 were administered on days −1, 1, 3, and 4 after DSS cessation in tandem with combination ICIs on days 0, 2, and 4 (n = 10 per group).

(D) Percent change in baseline body weight.

(E) DAI score.

(F) Colon length in millimeters.

(G) Histological damage scoring (n = 5 per group).

(H) Representative H&E-stained colon sections of ICI-treated mice with and without B cell depletion. Scale bars: 110 μm.

(I and J) Number of colonic T cells averaged per mm of colon with percent of cells expressing IL-17A, IFN-γ, and TNF-α (n = 5 per group). Experiments were repeated three times with similar results.

Mean ± SEM; ANOVA tests with Tukey post hoc or Bonferroni correction for multiple comparisons. ns: no significance, *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.