Figure 1.
IgH.TEμ CLL mouse model recapitulates key features of the human pathology. Aging mouse cohorts of IgH.TEμ transgenic mice and wild-type (WT) littermate control animals were monitored over time for disease development and progression and analyzed at end-stage. (A) Representative flow cytometric profiles of splenocytes stained for CD19, B220, CD5, and CD43 of WT littermate control and IgH.TEμ mice at indicated time points, 6 and 9 months (mos), are shown. The CD5 and CD43 histograms are gated on CD19+ B220+ B cells for WT control (dashed line, left) and on CD19+ B220+ (dashed line) and CD19+ B220− (solid line, center and right panels) for IgH.TEμ mice. (B) Kaplan-Meier survival curves of WT (blue line, n = 10) and IgH.TEμ (red line, n = 16) aging cohorts. (C) Macroscopic view of representative tissues: 1 liver lobe, spleen, femurs, and lymph nodes (LN) derived from WT and IgH.TEμ mice at end-stage (9 months LN; 10 months spleen, liver, and femur) is depicted. Absolute cell numbers of CD19+ cells (D) in the spleen and (E) mesenteric LN (mesLN) of WT littermates (blue circles, n = 5) and IgH.TEμ mice (red squares, n = 6) are displayed. P values were calculated using unpaired Student t test: **P = .0026, *P = .0150. (F) May Grunwald-Giemsa staining of cytospin preparations of splenocytes from WT littermate control (left) and IgH.TEμ mice (right) at 7 months. Arrows point to the larger and more folded nuclei of B lymphocytes in splenocytes of IgH.TEμ mice. (G) Hematoxylin and eosin staining of spleen and axillary LN (axLN) sections from WT littermate control (upper) and IgH.TEμ mice (lower) at 7 months. Scale bars as indicated.