原创力文档specific post-translational histone modifications of neutrophil extracellular traps as immunogens and potential targets of lupus autoantibodies具体翻译后组蛋白修饰的嗜中性粒细胞胞外陷阱狼疮自身抗体的免疫原和潜在的目标.pdfVIP
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specific post-translational histone modifications of neutrophil extracellular traps as immunogens and potential targets of lupus autoantibodies具体翻译后组蛋白修饰的嗜中性粒细胞胞外陷阱狼疮自身抗体的免疫原和潜在的目标
Liu et al. Arthritis Research Therapy 2012, 14:R25
/content/14/1/R25
RESEARCH ARTICLE Open Access
Specific post-translational histone modifications
of neutrophil extracellular traps as immunogens
and potential targets of lupus autoantibodies
1,4 1 1 1 2
Chih Long Liu , Stephanie Tangsombatvisit , Jacob M Rosenberg , Gil Mandelbaum , Emily C Gillespie ,
Or P Gozani4, Ash A Alizadeh3* and Paul J Utz1*
Abstract
Introduction: Autoreactivity to histones is a pervasive feature of several human autoimmune disorders, including
systemic lupus erythematosus (SLE). Specific post-translational modifications (PTMs) of histones within neutrophil
extracellular traps (NETs) may potentially drive the process by which tolerance to these chromatin-associated
proteins is broken. We hypothesized that NETs and their unique histone PTMs might be capable of inducing
autoantibodies that target histones.
Methods: We developed a novel and efficient method for the in vitro production, visualization, and broad profiling
of histone-PTMs of human and murine NETs. We also immunized Balb/c mice with murine NETs and profiled their
sera on autoantigen and histone peptide microarrays for evidence of autoantibody production to their
immunogen.
Results: We confirmed specificity toward acetyl-modified histone H2B as well as to other histone PTMs in sera
from patients with SLE known to have autoreactivity against histones. We observed enrichment for distinctive
histone marks of transcriptionally silent DNA during NETosis triggered by diverse stimuli. However, NETs derived
from human and murine sources did not harbor many of the PTMs toward which autoreactivity was observed in
patients with SLE or in MRL/lpr mice. Further, whil
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