Faculty, Kellogg School of Science and Technology
Receptor Editing In B Lymphocytes
The immune system eliminates lymphocytes with antigen receptors reactive to self-tissue and promotes the proliferation of cells that respond to foreign substances. We have discovered that one way that autoreactive lymphocytes are eliminated is not through cell death, but through an induced alteration of their antigen receptor genes. During their development in the bone marrow, immature B cells whose receptors bind antigens renew rearrangement of the genes for antibody light chains, allowing the cells to alter their antigen receptors and to lose self-reactivity. This process, called "receptor editing", is apparently controlled at the level of recombinase genes (RAGs). Recombinase genes can also become reactivated during the immune response to foreign antigens. We are currently trying to understand how signals from the antigen receptor can control recombinase and how this regulation is rewired at different stages of development.
Ph.D., Harvard University, 1983
B.A. Biochemistry, cum laude Harvard College, 1979
Ph.D. Cellular and Developmental Biology, Harvard University 1983
Scientific Member, Basel Institute for Immunology, Basel, Switzerland 1983-89 Immunology
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Hertz, M. and Nemazee, D. (1997). BCR ligation induces receptor editing in lgM+D- bone marrow B-cells in vitro. Immunity 6, 429-436.
Melamed, D., Benschop, R.J., Cambier, J.C., and Nemazee, D. (1998). Developmental regulation of B lymphocyte immune tolerance compartmentalizes clonal selection from receptor selection. Cell, 92, 173-182.
Hertz M., Kouskoff, V., Nakamura, T., and Nemazee, D. (1998). V (D)J recombinase induction in splenic B cells is inhibited by antigen receptor ligation. Nature, 394, 292-295.