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. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: Eur J Immunol. 2015 Sep 23;45(11):2978–2984. doi: 10.1002/eji.201445146

Figure 3. BCR signaling strength governs B-cell subset fate and progression to leukemia.

Figure 3

A. Generation of different B-cell subsets governed by BCR signal strength. The ATA μκTg mouse line on a Thy-1 knockout background (ATAμκTg.ThyKO) was crossed with lck-Thy-1 transgenic mouse lines expressing different levels of Thy-1 (from higher than normal level, wildtype level, lower, lowest, and completely absent). High levels promote the B1 cell fate from B-1 development, while very low levels generate MZ B cells and FO B-cell maturation occurs in the absence of Thy-1. B. In mice expressing VH3609μ at the pre-B-cell stage, expression of different light chains results in the generation of different B-cell subsets, either B1 from B-1 development or MZ B (and some FO B cells) from B-2 development. These BCRs have different autoreactivity but both can produce autoantibody, as natural autoreactive B cells: ATA, anti-thymocyte autoantibody, and AGcA, anti-intestinal goblet cell/mucin 2 autoreactivity. We are now asking whether B cells in these different autoreactive subsets carry a similar risk of progression to CLL.