Supplementary Figure 5: Characterization of the TH17 response during CIA. | Nature Immunology

Supplementary Figure 5: Characterization of the TH17 response during CIA.

From: Regulation of autoantibody activity by the IL-23–TH17 axis determines the onset of autoimmune disease

Supplementary Figure 5

(a) Flow-cytometric analysis of the content of IL-17-expressing CD3+ T cells in spleen, inguinal lymph nodes (LN) and paws of wild-type (WT) DBA mice at indicated time points during the course of collagen-induced arthritis (CIA). (b) Mean percentage and fold change of the numbers as well as (c) total cells/organ of indicated T cell subsets in spleen, LN and paws of WT DBA/1 mice at indicated time points after induction of CIA. CD4+CD3+ T cells were subcategorized into IFNγ-expressing Th1 cells, IL-4-expressing Th2 cells, IL-17-expressing TH17 cells and FoxP3-expressing Treg cells. (d) Frequency of IL-17-positive, IL-22-positive and IL-17/IL-22 double-positive T cells in spleens and lymph nodes of WT mice at the indicated time points after induction of CIA. (e) Identification of CD4+Bcl-6+IL17+ T cells within germinal centers of the spleen 26 days after induction of CIA (f) Proposed model of the IL23/Th17-mediated control of autoantibody activity. (g) Flow cytometry-based quantification of the expression of the IL-22 receptor (IL22Rα1) on CD19+B220+ B cells that were differentiated into plasmablasts by incubation with LPS (5μg/ml). (h) Quantification of IL-22 receptor (IL-22Rα1) surface expression on splenic CD19+B220+ B cells at day 0 and day 26 after induction of CIA. (i) mRNA expression of IL22Ra1 in in vitro differentiating plasmacells. Error bars represent SEM*P < 0.05, **P < 0.01, ***P < 0.001; Student’s t test. Error bars represent SEM*P < 0.05, **P < 0.01, ***P < 0.001; Student’s t test.

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