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Cellular & Molecular Immunology 2019年第7期16卷 671-673页

作者： Hussein Issaoui Nour Ghazzaui Mélissa Ferrad françois boyer Yves Denizot UMR CNRS 7276 INSERM U1262Equipe Labellisée LIGUE 2018University of LimogesCBRSrue Pr.Descottes87025 LimogesFrance

After encountering antigen,B-cells undergo class switch recombination(CSR)that substitutes the constant(C)μgene with Cγ,Cε,or Cα,thereby generating IgG,IgE,and IgA antibodies with new effector functions but the same antigenic specificity.1 The DNA-editing enzyme activation-induced deaminase(AID)is required for CSR by targeting specific DNA switch(S)regions preceding the C region,except Cδ.2 Sμis the donor region,while Sγ,ε,αare the acceptor regions.CSR is controlled in cis by the immunoglobulin heavy chain(IgH)3’regulatory region(3’RR).3 The 3’RR is essential to poise AID on the S acceptor region.During CSR IgH,intrachromosomal interactions(schematized in Fig.1a)are found between the 3’RR and the intronic Eμenhancer.1,4 Looping allows transcriptional binding activators to enhancers to facilitate CSR.However,CSR is only modestly influenced by Eμdeletion.5–7 During CSR,two different DNA repair pathways take place:the classical nonhomologous end joining(c-NHEJ)and the alternative end joining(A-EJ)pathways.

关键词： joining thereby generating

High-throughput sequencing reveals similar molecular signatures for class switch recombination junctions for theγandαisotypes

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Cellular & Molecular Immunology 2019年第1期16卷 90-92页

作者： ussein Issaoui Nour Ghazzaui Alexis Saintamand Yves Denizot françois boyer UMR CNRS 7276 INSERM U1262CBRSLimoges Universityrue Pr.DescottesLimoges 87025France INSERM U1236 Rennes 1 UniversityRennesFrance

INTRODUCTION After encountering an antigen,B cells undergo class switch recombination(CSR),which substitutes the Cμgene with Cγ,Cε,or Cαto generate IgG,IgE,and IgA antibodies with the same antigenic specificity but new effector functions.1 The DNAediting enzyme activation-induced deaminase(AID)is essential for CSR by targeting switch(S)regions preceding Cμ(namely,the Sμdonor region)and the Cγ,Cε,and Cαgenes(namely,the Sγ,ε,αacceptor regions).1 Cis-and trans-controlled DNA double strand beaks are generated during this process.2–6 Recruitment of DNA repair factors that facilitate the end-joining process is a crucial step of class switch recombination.Two pathways are implicated in this end joining.The classical non-homogenous end joining(c-NHEJ)pathway ligates DNA ends with no or little homology.By contrast,the alternative end joining(A-EJ)pathways is used to ligate DNA ends that have microhomology.

关键词： functions. process. joining

Uracil-DNA glycosylase is not implicated in the choice of the DNA repair pathway during B-cell class switch recombination

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Cellular & Molecular Immunology 2019年第1期16卷 93-95页

作者： Nour Ghazzaui Hussein Issaoui Alexis Saintamand Yves Denizot françois boyer UMR CNRS 7276 INSERM U1262University of LimogesCBRSrue Pr.Descottes87025 LimogesFrance INSERM U1236 Rennes 1 UniversityRennesFrance

Mature B-cells express membrane IgM and IgD(of same specificity)through alternative splicing of a pre-mRNA encompassing constant(C)μand Cδgenes.After encountering antigen,Bcells undergo class switch recombination(CSR)that substitutes the Cμgene with Cγ,Cε,or Cα,thereby generating IgG,IgE,and IgA antibodies with the same antigenic specificity but new effector functions.DNA-editing enzyme activation-induced deaminase(AID)is essential for CSR by targeting switch(S)regions preceding Cμ(namely,the Sμdonor region)and the Cγ,Cε,and Cαgenes(namely,the Sγ,ε,αacceptor regions).1,2 CSR is controlled in cis by IgH locus super-enhancers3 and in trans by a wide spectrum of enzymes and proteins.1,2 Among them,the role of the uracil DNA glycosylase(UNG)remains controversial.UNG is a key enzyme of base excision repair,which carries out faithful repair.Some authors estimate that during CSR,the UNG enzymatic activity removes the AID-induced dC to dU converted base of singlestrand DNA,generating abasic sites and leading to DNA strand breaks.1 For other authors,the role of UNG is to stabilize the S–S synapse and to recruit DNA repair factors that facilitate the endjoining process.4,5 Thus,the classical non-homogenous end joining pathway would be increased over the alternative end joining(A-EJ)pathway in UNG-deficient mice,4 suggesting an intriguing role of UNG in promoting the A-EJ pathway.

关键词： generating joining specificity

IgD class switch recombination is not controlled through the immunoglobulin heavy chain 3′ regulatory region super-enhancer

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Cellular & Molecular Immunology 2017年第10期14卷 871-874页

作者： Hussein Issaoui Nour Ghazzaui Alexis Saintamand Yves Denizot françois boyer UMR CNRS 7276 University of LimogesCBRS87025 LimogesFrance Present address:INSERM U1236 UniversitéRennes 1RennesFrance

In secondary lymphoid organs,mature B cells express membrane immunoglobulin(Ig)of M and D isotypes(IgM and IgD,respectively)of the same specificity through alternative splicing of a pre-mRNA encompassing the VDJ variable region and Cμand Cδheavy chain constant exons.1 After encountering antigen,B cells undergo class switch recombination(CSR)by which the Cμgene is substituted with Cγ,Cεor Cα,thereby generating IgG,IgE and IgA antibodies of the same antigenic specificity but with new effector functions.CSR requires the DNA-editing enzyme activation-induced deaminase(AID).

关键词： functions. substituted thereby

IgH locus suicide recombination does not depend on NHEJ in contrast to CSR in B cells

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Cellular & Molecular Immunology 2019年第2期16卷 201-202页

作者： Hend Boutouil françois boyer Jeanne Cook-Moreau Michel Cogné Sophie Péron CRIBL UMR CNRS 7276 INSERM U126287000 LimogesFrance Institut Universitaire de france 75000 ParisFrance

IgH locus suicide recombination(LSR)occurs in activated Blymphocytes and may result in the death of the concerned B cell,justifying the name“locus suicide recombination”.1 LSR,as for immunoglobulin(Ig)class switch recombination(CSR),is an intrachromosomal recombination in the Ig heavy chain(IgH)locus.Nevertheless,LSR somehow appears to be the detrimental counterpart of CSR in activated B cells,since CSR intends for cells to actively participate in immune responses while LSR eliminates B cells.Therefore,an important question to address is the regulation and the exact molecular mechanism of LSR.

关键词： CSR eliminate concerned

Molecular analysis of γ1, γ3, and α class switch recombination junctions in APOBEC3-deficient mice using high-throughput sequencing

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Cellular & Molecular Immunology 2020年第4期17卷 418-420页

作者： Hussein Issaoui Mélissa Ferrad Nour Ghazzaui Sandrine Lecardeur Jeanne Cook-Moreau françois boyer Yves Denizot UMR CNRS 7276 INSERM U1262Equipe Labellisée LIGUE 2018University of LimogesCBRSrue Pr.Descottes87025 LimogesFrance

Activation-induced deaminase(AID)is required for immunoglobulin(Ig)class switch recombination(CSR),in which the constant(C)μgene of IgM is substituted with C_(γ),C_(ε),or C_(α),thereby generating IgG,IgE,and IgA antibodies,respectively,with new effector functions but the same antigenic specificity.1 AID targets specific DNA switch(S)regions preceding C regions except for Cδ.2 Sμis usually the donor region,while Sγ,ε,αare the acceptor regions.AID deaminates C into U on single-stranded DNA by targeting the WRCY(W=A/T,R=A/G,and Y=C/T)hot motif and,to a lesser extent,the SYC(S=G/C,Y=C/T)cold motif.3,4 AID is a member of the apolipoprotein B editing complex(APOBEC)family.Among APOBEC genes,a family of evolutionarily conserved cytidine deaminases,APOBEC3 is implicated in diverse cell functions including innate immunity against retroviruses.4 The DNA-editing APOBEC3 enzymes have recently attracted attention due to their involvement in cancer and potential applications in gene editing.5–7 While a single copy of each APOBEC3 gene is present in rodents,seven copies of each APOBEC3 gene are found in humans.

关键词： immunity involvement thereby

Mediator contributes to IgH locus VDJ rearrangements by promoting usage of most distal V segments

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Cellular & Molecular Immunology 2020年第4期17卷 407-409页

作者： Iman Dalloul Zeinab Dalloul Sandrine Le Noir françois boyer Bernardo Reina-San-Martin Jeanne Cook-Moreau Michel Cogné UMR CNRS 7276 INSERM U1262Universite de LimogesLimoges 87025France INSERM U1258 UMR CNRS 7104Institut de Genetique et de Biologie Moleculaire et CellulaireUniversitéde StrasbourgIllkirch 67400France

INTRODUCTION The immunoglobulin heavy(IgH)chain locus includes a large cluster of V,D and J segments spanning thousands of kilobases in mammals and its expression implies long-range 3D-regulation of various gene modifications.1 V(D)J recombination occurs during early B-cell ontogeny.2 It is regulated by multiple transcription factors and cis-regulatory elements,and most notably by the intronic 5′Eμelement located in the JH to Cμintron.3 The intergenic control region 1(IGCR1)located between the VH and D gene clusters inhibits rearrangement of the most DH-proximal VH gene segments,while promoting usage of distal VH gene segments.4 Other downstream elements of the locus,flanking its 3′end might have more subtle roles:while the large 3′regulatory region(3′RR)shows strong internal synergies2 and behaves as a superenhancer in mature B cells.Its deletion showed no influence on the VDJ repertoire and rather increased transcription of unrearranged V segments.3–5 Insulators binding CTCF farther downstream of the 3′RR were shown,however,to promote usage of distal VH segments.6 Altogether,there are strong indications that elements involved in long-distance regulation of transcription might also influence VDJ recombination.In-frame splicing of VDJ exons is also needed for full Ig expression.7 Given the functional importance of gene architecture and long-range interactions for the IgH locus physiology,we explored the dependence of the VDJ repertoire on Med1,a known actor of long-range enhancer interactions.

关键词： B cells mediator VDJ repertoire

Trans-silencing effect of the 3′RR immunoglobulin heavy chain enhancer on Igκtranscription at the pro-B cell stage

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Cellular & Molecular Immunology 2019年第7期16卷 668-670页

作者： Nour Ghazzaui Hussein Issaoui Ophélie Alyssa Martin Alexis Saintamand Jeanne Cook-Moreau Yves Denizot françois boyer CNRS UMR 7276 Inserm U1262Universitéde LimogesLimogesFrance Present address:Inserm U1236 UniversitéRennes 1RennesFrance

Due to their impact on nuclear organization,enhancers are master regulators of cell fate.1,2 The immunoglobulin heavy chain(IgH)locus undergoes numerous changes(such as transcription,accessibility,DNA breaks,and mutations)throughout B-cell differentiation.Several of these events are controlled by the IgH 3′regulatory region(3′RR).The 3′RR is the master control element of mature B-cell IgH transcription,3 somatic hypermutation(SHM),4,5 conventional class switch recombination(CSR),4,6–10 and locus suicide recombination(LSR).11 In contrast,the 3′RR is expected to be dispensable for V(D)J recombination.12,13 During Bcell development,the heavy and light chain loci are poised for their VDJ and VJ rearrangements,respectively.The IgH locus rearranges first,with D-J joining at the pro-B-cell stages,followed by V-DJ joining at the pre-B-cell stage.The Igk locus is poised for VJ rearrangements at the pre-B cell stage.

关键词： effect joining recombination

Reproducing indolent B-cell lymphoma transformation with T-cell immunosuppression in LMP1/CD40-expressing mice

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Cellular & Molecular Immunology 2019年第4期16卷 412-414页

作者： Christelle Vincent-Fabert Alexis Saintamand Amandine David Mehdi Alizadeh françois boyer Nicolas Arnaud Ursula Zimber-Strobl Jean Feuillard Nathalie Faumont CNRS-UMR 7276 INSERM U1262 CRIBL University of Limogesand Hematology Laboratory of Dupuytren Hospital University Center(CHU)of LimogesLimogesFrance INSERM U917 University of Rennes 1RennesFrance LNPRM EFS BretagneRennesFrance Research Unit Gene Vectors Helmholtz Center MunichGerman Research Center for Environmental Health GmbHMunichGermany

Indolent B-cell lymphomas are a group of incurable cancers of the elderly that encompass various entities,such as chronic lymphocytic leukemia(CLL),follicular lymphoma(FL),and marginal zone lymphoma(MZL).All indolent lymphomas may evolve towards aggressive transformation with an increased proliferation index and decreased tumor doubling time.This transformation,which is called Richter’s syndrome in CLL,is associated with an aggressive clinical course and poor survival.At least in CLL,transformation of an indolent B-cell clone is molecularly different from that of de novo diffuse large B-cell lymphomas.1 Aging is known to be associated with immune decline,with increased inflammation,decreased immune surveillance and increased onset of malignancies among the consequences.2 Progression of indolent B-cell lymphomas is likely to be associated with escape from immune surveillance.

关键词： lymphoma Richter transformation

Retraction Note:3′RR and 5′Eμimmunoglobulin heavy chain enhancers are independent engines of locus remodeling

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Cellular & Molecular Immunology 2021年第8期18卷 2082-2082页

作者： Nour Ghazzaui Hussein Issaoui françois boyer Ophélie Alyssa Martin Alexis Saintamand Yves Denizot CNRS UMR 7276 Inserm U1262Universitéde LimogesLimogesFrance Present address:Inserm U1236 UniversitéRennes 1RennesFrance

The authors have retracted this Correspondence.After the publication of this correspondence,it came to the authors’attention that the control RAG2^(−/−)mouse was a RAG2^(−/−)γc^(−/−)mouse.This point resulted in the ... 详细信息

关键词： journal correspondence conclusions