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10.1016/j.immuni.2015.10.002

http://scihub22266oqcxt.onion/10.1016/j.immuni.2015.10.002
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C4654975!4654975!26546282
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suck abstract from ncbi


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pmid26546282      Immunity 2015 ; 43 (5): 884-95
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  • Activation-induced cytidine deaminase (AID) expression in human B-cell precursors is essential for central B-cell tolerance #MMPMID26546282
  • Cantaert T; Schickel JN; Bannock JM; Ng YS; Massad C; Oe T; Wu R; Lavoie A; Walter JE; Notarangelo LD; Al-Herz W; Kilic SS; Ochs HD; Nonoyama S; Durandy A; Meffre E
  • Immunity 2015[Nov]; 43 (5): 884-95 PMID26546282show ga
  • Activation-induced cytidine deaminase (AID), the enzyme mediating class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes, is essential for the removal of developing autoreactive B cells. How AID mediates central B-cell tolerance remains unknown. We report that AID enzymes were produced in a discrete population of immature B cells that expressed recombination-activating gene 2 (RAG2), suggesting that they undergo secondary recombination to edit autoreactive antibodies. However, most AID+ immature B cells lacked anti-apoptotic MCL-1 and were deleted by apoptosis. AID inhibition using lentiviral-encoded short hairpin (sh)RNA in B cells developing in humanized mice resulted in a failure to remove autoreactive clones. Hence, B-cell intrinsic AID expression mediates central B-cell tolerance potentially through its RAG-coupled genotoxic activity in self-reactive immature B cells.
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