Germinal center dysregulation by histone methyltransferase EZH2 promotes lymphomagenesis.

Protection against deadly pathogens requires the production of high-affinity antibodies by B cells, which are generated in germinal centers (GCs). Alteration of the GC developmental program is common in many B cell malignancies. Identification of regulators of the GC response is crucial to develop t...

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Publicado en:Journal of Clinical Investigation Vol. 123; no. 12; pp. 5009 - 5023
Autores principales: Caganova, Marieta, Carrisi, Chiara, Varano, Gabriele, Mainoldi, Federica, Zanardi, Federica, Germain, Pierre-Luc, George, Laura, Alberghini, Federica, Ferrarini, Luca, Talukder, Asoke K, Ponzoni, Maurilio, Testa, Giuseppe, Nojima, Takuya, Doglioni, Claudio, Kitamura, Daisuke, Toellner, Kai-M, Su, I-Hsin, Casola, Stefano
Formato: research Journal Article
Publicado: American Society for Clinical Investigation Dec2013
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Dec2013
      vid: 123
      iid: 12
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      pub: American Society for Clinical Investigation
      place: Ann Arbor, Michigan
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        atl: Germinal center dysregulation by histone methyltransferase EZH2 promotes lymphomagenesis.
      aug:
        au:
          Caganova, Marieta
          Carrisi, Chiara
          Varano, Gabriele
          Mainoldi, Federica
          Zanardi, Federica
          Germain, Pierre-Luc
          George, Laura
          Alberghini, Federica
          Ferrarini, Luca
          Talukder, Asoke K
          Ponzoni, Maurilio
          Testa, Giuseppe
          Nojima, Takuya
          Doglioni, Claudio
          Kitamura, Daisuke
          Toellner, Kai-M
          Su, I-Hsin
          Casola, Stefano
      sug:
        subj:
          B Lymphocytes Immunology
          Lymphoid Tissue
          Lymphoma, Non-Hodgkin's Etiology
          Proteins Physiology
          Animal Studies
          Antibody Formation
          Apoptosis
          B Lymphocytes Pathology
          Biochemical Phenomena
          Cell Cycle
          DNA
          Genes
          Genetics
          Hematopoiesis
          Hydrolases
          Hydrolases Deficiency
          Hydrolases Physiology
          Immunity
          Lymphoid Tissue Immunology
          Lymphoid Tissue Pathology
          Lymphoma, Non-Hodgkin's
          Lymphoma, Non-Hodgkin's Pathology
          Methylation
          Mice
          Proteins
          Funding Source
      ab: Protection against deadly pathogens requires the production of high-affinity antibodies by B cells, which are generated in germinal centers (GCs). Alteration of the GC developmental program is common in many B cell malignancies. Identification of regulators of the GC response is crucial to develop targeted therapies for GC B cell dysfunctions, including lymphomas. The histone H3 lysine 27 methyltransferase enhancer of zeste homolog 2 (EZH2) is highly expressed in GC B cells and is often constitutively activated in GC-derived non-Hodgkin lymphomas (NHLs). The function of EZH2 in GC B cells remains largely unknown. Herein, we show that Ezh2 inactivation in mouse GC B cells caused profound impairment of GC responses, memory B cell formation, and humoral immunity. EZH2 protected GC B cells against activation-induced cytidine deaminase (AID) mutagenesis, facilitated cell cycle progression, and silenced plasma cell determinant and tumor suppressor B-lymphocyte-induced maturation protein 1 (BLIMP1). EZH2 inhibition in NHL cells induced BLIMP1, which impaired tumor growth. In conclusion, EZH2 sustains AID function and prevents terminal differentiation of GC B cells, which allows antibody diversification and affinity maturation. Dysregulation of the GC reaction by constitutively active EZH2 facilitates lymphomagenesis and identifies EZH2 as a possible therapeutic target in NHL and other GC-derived B cell diseases.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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