Faculty Summaries
Kyoko Hayakawa, MD, PhD
Kyoko Hayakawa, MD, PhD
Office Phone: 215-728-5362
Lab Phone: 215-728-5362
Fax: 215-728-3574
Lab: R388
  • Lab Overview

    B1 B cells generated early in life by fetal/neonatal B-1 development in mice include autoreactive cells with detectable CD5 upregulation induced by BCR signaling. Part of such early-generated B1 B cells are maintained by self-renewal for life, continuously providing auto- and poly-reactive antibodies, serving a protective role. However, the B1 B cell subset has a higher risk of dysregulated growth and progression to chronic lymphocytic leukemia (CLL)/lymphoma during aging, than other B cell subsets.

    We have generated several autoreactive germline gene BCR models that enable comparison of B cells generated under conditions of natural exposure to autoantigen for such studies. Analysis of these mice has been key in understanding the importance of BCR and BCR signaling for generation of different B cell subsets and in investigating the cellular origin of CLL. Early generated B1 B cells can circulate, and are constantly exposed to the microenvironment, promoting life-long self-renewal. Thus, in addition to the importance of B cell origin, BCR signaling, and genetic background influences, the role of the microenvironment is another important issue for understanding how B1 cells progress to become CLL.