Journal
IMMUNOLOGY LETTERS
Volume 135, Issue 1-2, Pages 74-77Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.imlet.2010.09.018
Keywords
Receptor editing; Tonic BCR signaling
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Funding
- NIH [R01 AR043805]
- Leukemia and Lymphoma Society
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Light chain receptor editing is an important mechanism that prevents B cell self-reactivity. We have previously shown that tonic signaling through the BCR represses RAG expression at the immature B cell stage, and that initiation of light chain rearrangements occurs in the absence of these tonic signals in an in vitro model of B cell development. To further test our hypothesis we studied the effect of itpkb deficiency (irpkb(-/-) mice) or Raf hyper-activation (Raf-CAAX transgenic mice), two mutations that enhance BCR signaling, on receptor editing in an in vivo model. This model relies on transferring bone marrow from wild-type or mutant mice into mice expressing an anti-kappa light chain transgene. The anti-kappa transgene induces receptor editing of all kappa light chain expressing B cells, leading to a high frequency of lambda light chain expressing B cells. Anti-kappa transgenic recipients of bone marrow from itpkb(-/-) or Raf-CAAX mice showed lower levels of editing to lambda light chain than did non-transgenic control recipients. These results provide evidence in an in vivo model that enhanced BCR signaling at the immature B cell stage of development suppresses light chain receptor editing. (C) 2010 Elsevier B.V. All rights reserved.
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