Population‐Specific Patterns of Epigenetic Defects in the B Cell Lineage in Patients With Systemic Lupus Erythematosus.

Objective: To determine the stage of B cell development at which a systemic lupus erythematosus (SLE)–associated DNA methylation signature originates in African American (AA) and European American (EA) subjects, and to assess whether epigenetic defects in B cell development patterns could be predict...

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Publicado en:Arthritis & Rheumatology Vol. 72; no. 2; pp. 282 - 292
Autores principales: Breitbach, Megan E., Ramaker, Ryne C., Roberts, Kevin, Kimberly, Robert P., Absher, Devin
Formato: research tables/charts Journal Article
Publicado: Wiley-Blackwell Feb2020
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Feb2020
      vid: 72
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1002/art.41083
        141451150
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        atl: Population‐Specific Patterns of Epigenetic Defects in the B Cell Lineage in Patients With Systemic Lupus Erythematosus.
      aug:
        au:
          Breitbach, Megan E.
          Ramaker, Ryne C.
          Roberts, Kevin
          Kimberly, Robert P.
          Absher, Devin
        affil: University of Alabama at Huntsville and HudsonAlpha Institute for Biotechnology
      sug:
        subj:
          Epigenomics
          Lupus Erythematosus, Systemic Risk Factors
          Cell Differentiation
          B Lymphocytes
          Genes
          African Americans
          White Persons
          DNA Methylation
          Transcription Factors
          Algorithms
          Regression
          Interferons
          ROC Curve
          Female
          Ethnic Groups
          Race Factors
          Human
          Female
      ab: Objective: To determine the stage of B cell development at which a systemic lupus erythematosus (SLE)–associated DNA methylation signature originates in African American (AA) and European American (EA) subjects, and to assess whether epigenetic defects in B cell development patterns could be predictive of SLE status in individual and mixed immune cell populations. Methods: B cells from AA patients (n = 31) and EA patients (n = 49) with or without SLE were sorted using fluorescence‐activated cell sorting into 5 B cell subsets. DNA methylation, measured at ~460,000 CpG sites, was interrogated in each subset. Enrichment analysis of transcription factor interaction at SLE‐associated methylation sites was performed. A random forests algorithm was used to identify an epigenetic signature of SLE in the B cell subsets, which was then validated in an independent cohort of AA and EA patients and healthy controls. Results: Regression analysis across all B cell stages resulted in identification of 60 CpGs that reached genome‐wide significance for SLE‐associated methylation differences (P ≤ 1.07 × 10−7). Interrogation of ethnicity‐specific CpGs associated with SLE revealed a hypomethylated pattern that was enriched for interferon (IFN)–regulated genes and binding of EBF1 in AA patients (each P < 0.001). AA patients with SLE could be distinguished from healthy controls when the predictive model developed with the transitional B cell subset was applied to other B cell subsets (mean receiver operating characteristic [ROC] area under the curve [AUC] 0.98), and when applied to CD19+ pan–B cells (mean ROC AUC 0.95) and CD4+ pan–T cells (mean ROC AUC 0.97) from the independent validation cohort. Conclusion: These results indicate that SLE‐specific methylation patterns are ethnicity dependent. A pattern of epigenetic changes near IFN‐regulated genes early in B cell development is a hallmark of SLE in AA female subjects. EBF1 binding sites are highly enriched for significant methylation changes, implying that this may be a potential regulator of SLE‐associated epigenetic changes.
      pubtype: Academic Journal
      doctype:
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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