Fig. 3: TNIP1-driven cellular phenotypes are dependent on MyD88 signaling.
From: A TNIP1-driven systemic autoimmune disorder with elevated IgG4

a–f, Representative flow cytometry plots and proportions of splenocytes from male (n = 12, dots) and female (n = 17, triangles) vikala mice aged 16–20 weeks: GC B cells (CD19+CD95+BCL6+) (a); PCs (CD138+CD98+) (b); ABCs (B220+CD21−CD23−CD19highCD11c+) (c); switched B cells (B220+CD21−CD23−IgD−IgM−) (d); TFH cells (CD4+CXCR5+PD1high) (e); and extrafollicular TH cells (CD4+CXCR5−PD1+CXCR3+) (f), either competent or deficient in Myd88. Tnip1+/+ (n = 6), Tnip1vik/+ (n = 8), Tnip1vik/vik (n = 6), Tnip1vik/+ Myd88−/− (n = 6) and Tnip1vik/vik Myd88−/− (n = 3). The bars represent the median values; each point represents an individual mouse (biological replicate). g, serum IgG2c antibodies in 16–20-week-old vikala mice either competent or deficient in Myd88; Tnip1+/+ (n = 9), Tnip1vik/+ (n = 9), Tnip1vik/vik (n = 9), Tnip1vik/+ Myd88−/− (n = 6) and Tnip1vik/vik Myd88−/− (n = 3). The black lines represents the median; each point represents an individual mouse (biological replicate); sex is indicated by the respective symbol. h, Serum antibodies to DNA (ANAs) in 16–20-week-old vikala mice either competent or deficient in Myd88; Tnip1+/+ (n = 8), Tnip1vik/+ (n = 12), Tnip1vik/vik (n = 9), Tnip1vik/+ Myd88−/−(n = 6) and Tnip1vik/vik Myd88−/− (n = 3). The bars represent the median; each point represents an individual mouse (biological replicate). In a–f, data are representative of n = 2 independent experiments. In g,h, data are from experiments performed once. Statistical significance was performed using a one-way ANOVA with Tukey’s correction for multiple comparison after log-transformation of data. Exact P values are shown.