Loss of IRF-4–binding protein leads to the spontaneous development of systemic autoimmunity
J. Clin. Invest. Jessica C. Fanzo, et al. 116:703 doi:10.1172/JCI24096 [Go to this article.]

Figure 1
Lymphocyte development in IBP^trap/trap mice. (A) IBP protein expression in IBP^+/+, IBP^+/trap, and IBP^trap/trap splenocytes and thymocytes. Total cell lysates (20 μg) were prepared from splenocytes and thymocytes and probed with an anti-IBP antibody reactive against the C terminus of IBP (upper panel). Extracts from NIH 3T3 and EL4 cells were used as negative and positive controls, respectively. Reprobing with a β-actin antibody is shown as a loading control (lower panel). (B) Flow cytometric analysis of T lymphocyte populations from 6-week-old IBP^+/+ and IBP^trap/trap mice. Single-cell suspensions from thymus (upper panel), spleen (middle panel), and lymph nodes (lower panel) were stained with antibodies against CD4 and CD8. Percentages of positive cells within each quadrant are shown. (C) Flow cytometric analysis of B lymphocyte populations from 6-week-old IBP^+/+ and IBP^trap/trap mice. Single-cell suspensions from splenic B220⁺ cells were stained with antibodies against IgM and IgD (top panel) and CD23 and CD21 (middle panel). Bone marrow cells (lower panel) were stained with antibodies against IgM and B220 and gated to show pro- and pre-, immature and mature B cells. Percentages of positive cells within each gate are shown.