简体中文

AC-22-胞浆极性/高尔基体样型

同义词 无 None
描述
在细胞浆两级，靠近细胞核的一侧呈现不连续斑点或颗粒样染色。其对应的靶抗原主要是高尔基体（Golgi）相关蛋白
Discontinuous cytoplasmic coarse speckled or granular perinuclear ribbon-like staining with polar distribution (e.g., to one side of the nucleus)
抗原相关性
巨蛋白/巨高尔基蛋白
giantin/macrogolgin, golgin-95/GM130, golgin-160, golgin-97, golgin-245

  • 临床相关性

    一级信息

    关于临床相关性和缩写列表

    Clinical Relevance

    First level information

    About Clinical Relevance & List of Abbreviations

  • ▶在少数患有多种疾病的个体中有检出。
    ▶用于检测针对高尔基体特异抗原的自身抗体的特异性免疫检测试剂目前尚未商品化[1]。



    ▶Found in small numbers of individuals with a variety of conditions.
    ▶Specific immunoassays to detect autoantibodies directed to specific Golgi antigens are currently not commercially available [1].
  • 二级信息
    Second level information
  • ▶AC-22核型已在少数有多种病症的患者中报道，包括干燥综合征、系统性红斑狼疮、类风湿性关节炎、混合型结缔组织病、肉芽肿性血管炎、特发性小脑共济失调、副肿瘤性小脑变性、成人斯蒂尔氏病，以及病毒感染，包括HIV和EBV[1-5]。
    ▶尽管可能会受到转诊模式的影响，一项研究得出结论，AC-22核型在临床上与系统性自身免疫性风湿疾病无关[3,6]。另一项研究中，过半抗高尔基体阳性者为非自身免疫病，尤以肝病多见[7]。
    ▶AC-22核型在一般人群中很少见[8]。
    ▶The AC-22 pattern has been reported in small numbers of patients with a variety of conditions, including Sjögren’s disease (SjD), systemic lupus erythematosus, rheumatoid arthritis (RA), mixed connective tissue disease, granulomatosis with polyangiitis, idiopathic cerebellar ataxia, paraneoplastic cerebellar degeneration, adult Still’s disease, and viral infections including human immunodeficiency virus and Epstein-Barr virus [1-5].
    ▶Although possibly biased by the referral pattern, two studies concluded that the AC-22 pattern is not clinically associated with systemic autoimmune rheumatic diseases [3, 6]. In another study over half of the anti-Golgi positive cases had non-autoimmune diseases, but particularly had hepatic disorders [7].
    ▶The AC-22 pattern is rare in the general population [8].
  • 参考文献
  • 1.Stinton LM, Eystathioy T, Selak S, Chan EKL, Fritzler MJ. Autoantibodies to protein transport and messenger RNA processing pathways: endosomes, lysosomes, Golgi complex, proteasomes, assemblyosomes, exosomes, and GW bodies. Clin Immunol. 2004;110:30-44.
    2.Fritzler MJ, Etherington J, Sokoluk C, Kinsella TD, Valencia DW. Antibodies from patients with autoimmune disease react with a cytoplasmic antigen in the Golgi apparatus. J Immunol. 1984;132:2904-8.
    3.Vermeersch P, Van den Bergh K, Blockmans D, Westhovens R, Bossuyt X. Anti-Golgi autoantibodies are not clinically associated with systemic autoimmune diseases. Ann Rheum Dis. 2011;70:234-5.
    4.Staub HL, Souza F, Chan EKL, von Muhlen CA. Anti-Golgi antibodies in adult Still's disease. Clin Exp Rheumatol. 2003;21:275-6.
    5.Zhai J, Liao J, Wang M, Huang Z, Hu J, Xu H, Xie Q, Ma B, et al. Anti-Golgi Antibody as a Potential Indicator for Rheumatoid Arthritis. Lab Med. 2022;53:156-60.
    6.Lee AYS, Culican S, Campbell D, Lin MW. Clinical associations of serum Golgi apparatus antibodies in an immunology laboratory cohort. Scand J Immunol. 2022;95:e13133.
    7.Hong HS, Chung WH, Hung SI, Chen MJ, Lee SH, Yang LC. Clinical association of anti-golgi autoantibodies and their autoantigens. Scand J Immunol. 2004;59:79-87.
    8.Satoh M, Chan EKL, Ho LA, Rose KM, Parks CG, Cohn RD, Jusko TA, Walker NJ, et al. Prevalence and sociodemographic correlates of antinuclear antibodies in the United States. Arthritis Rheum. 2012;64:2319-27.

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