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. 2018 Sep 13;9:1996. doi: 10.3389/fimmu.2018.01996

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Copyright © 2018 Pal Singh, de Bruijn, de Almeida, Meijers, Nitschke, Langerak, Pillai, Stadhouders and Hendriks.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Early onset of disease in VH11 expressing CLL from IgH.TEμ mice. (A) Bar graphs summarizing the distribution of CDR3 length in V_H11 (gray, n = 15) vs. non-V_H11 (white, n = 23) CLL from IgH.TEμ mice. (B) Web logo depicting stereotyped CDR3 amino acid sequence of V_H11 (n = 15) CLL from IgH.TEμ mice. (C) Retrospective Kaplan-Meier incidence curves including IgH.TEμ mice with identified V_H11 (dotted line) or non-V_H11 BCR CLL (solid line). (D–F) Histogram showing flow cytometric analysis of CD19⁺CD5⁺CD43⁺ splenic CLL cells from V_H11 (gray) vs. non-V_H11 (black line) CLL from IgH.TEμ mice, stained with (D) phosphatidylcholine (PtC) liposomes or fluorochrome conjugated (E) anti-IgM or (F) anti-IgD antibodies. Bar graphs summarize mean fluorescence intensity of V_H11 (gray) and non-V_H11 CLL (n = 6 per group).