V(D)J recombinase induction in splenic B lymphocytes is inhibited by antigen-receptor signalling

Marc Hertz, Valérie Kouskoff, Tetsuya Nakamura and David Nemazee ()
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Marc Hertz: National Jewish Medical and Research Center
Valérie Kouskoff: National Jewish Medical and Research Center
Tetsuya Nakamura: University of Tokyo, Institute of Medical Science
David Nemazee: National Jewish Medical and Research Center

Nature, 1998, vol. 394, issue 6690, 292-295

Abstract: Abstract In lymphocytes, DNA recombinations that generate the antigen-receptor genes can sometimes be reinduced in receptor-bearing cells in a process called receptor editing, which modifies the specificity of the receptor for antigen. In immature B lymphocytes, B-cell antigen receptor (BCR) signalling stimulates immune tolerance by receptor editing1,2,3,4,5. More mature splenic B cells can also be induced to undergo V(D)J recombination, which generates diversity in the immune system, either by immunization with foreign proteins6,7,8,9 or by stimulation in vitro with interleukin-4 and lipopolysaccharide8,9,10. Here we show that immune tolerance is unlikely to induce V(D)J recombination in mature B cells, because BCR ligation actively inhibits V(D)J recombination induced by interleukin-4 and lipopolysaccharide. Furthermore, immunization of immunoglobulin transgenic mice with ligands of varying avidities for the BCR showed that low-avidity antigen could induce strong V(D)J recombination, whereas non-binding or high-avidity ligands could not. These data suggest that V(D)J recombination induced during the immune response modifies the antigen receptors of B cells with weak, but not strong, reactivity to antigen, potentially rescuing cells with improved receptor affinity and promoting their contribution to the immune response. Thus BCR signalling regulates V(D)J recombination in both tolerance and immunity, but in strikingly different ways.

Date: 1998
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DOI: 10.1038/28419

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