<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-05-10T15:33:50Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/15126" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/15126</identifier><datestamp>2024-09-27T10:09:43Z</datestamp><setSpec>com_20.500.12105_19604</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19607</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Gómez-Escolar, Carmen</subfield>
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      <subfield code="a">Serrano-Navarro, Alvaro</subfield>
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      <subfield code="a">Benguria, Alberto</subfield>
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      <subfield code="a">Dopazo, Ana</subfield>
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      <subfield code="a">Sanchez-Cabo, Fatima</subfield>
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      <subfield code="a">Ramiro, Almudena R</subfield>
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      <subfield code="c">2022-10-07</subfield>
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      <subfield code="a">Germinal centers (GC) are microstructures where B cells that have been activated by antigen can improve the affinity of their B cell receptors and differentiate into memory B cells (MBCs) or antibody-secreting plasma cells. Here, we have addressed the role of activation-induced deaminase (AID), which initiates somatic hypermutation and class switch recombination, in the terminal differentiation of GC B cells. By combining single cell transcriptome and immunoglobulin clonal analysis in a mouse model that traces AID-experienced cells, we have identified a novel subset of late-prePB cells (L-prePB), which shares the strongest clonal relationships with plasmablasts (PBs). Mice lacking AID have various alterations in the size and expression profiles of transcriptional clusters. We find that AID deficiency leads to a reduced proportion of L-prePB cells and severely impairs transitions between the L-prePB and the PB subsets. Thus, AID shapes the differentiation fate of GC B cells by enabling PB generation from a prePB state.</subfield>
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      <subfield code="a">EMBO Rep . 2022 Oct 7;e55000. doi: 10.15252/embr.202255000.</subfield>
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      <subfield code="a">10.15252/embr.202255000</subfield>
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      <subfield code="a">1469-3178</subfield>
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      <subfield code="a">EMBO reports</subfield>
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      <subfield code="a">36205653</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/15126</subfield>
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   <datafield ind2="0" ind1="0" tag="245">
      <subfield code="a">Single cell clonal analysis identifies an AID-dependent pathway of plasma cell differentiation.</subfield>
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