Receptor editing explained

Receptor editing is a process that occurs during the maturation of B cells, which are part of the adaptive immune system. This process forms part of central tolerance to attempt to change the specificity of the antigen receptor of self reactive immature B-cells, in order to rescue them from programmed cell death, called apoptosis.[1] It is thought that 20-50% of all peripheral naive B cells have undergone receptor editing making it the most common method of removing self reactive B cells.[2]

During maturation in the bone marrow, B cells are tested for interaction with self antigens, which is called negative selection. If the maturing B cells strongly interact with these self antigens, they undergo death by apoptosis. Negative selection is important to avoid the production of B cells that could cause autoimmune diseases. They can avoid apoptosis by modifying the sequence of light chain V and J genes (components of the antigen receptor) so that it has a different specificity and may not recognize self antigens anymore. This process of changing the specificity of the immature B cell receptor is called receptor editing.

References

3. Kleinfield R, Hardy RR, Tarlinton, D (1986). 'Recombination between an expressed immunoglobulin heavy-chain gene and a germline variable gene segment in a Ly1+ B-cell lymphoma'. Nature 322 (6082): 843-6.

Notes and References

  1. Meffre, E . Wardemann, H . B-cell tolerance checkpoints in health and autoimmunity. . Current Opinion in Immunology . 20 . 632–638 . 2008 . 6 . 18848883 . 10.1016/j.coi.2008.09.001 .
  2. Halverson R, Torres RM, Pelanda R . Receptor editing is the main mechanism of B cell tolerance toward membrane antigens . Nature Immunology . 5 . 6. 645–650 . 2004 . 15156139 . 10.1038/ni1076 . 20869465 .