广西汉族多发性肌炎/皮肌炎与HLA-DQA1、-DQB1等位基因的相关性研究
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摘要
目的:研究广西汉族多发性肌炎/皮肌炎(PM/DM)与HLA-DQA1.-DQB1等位基因的相关性。
     方法:采用聚合酶链反应-序列特异性引物(Polymerase chain reaction-special sequence primers,PCR-SSP)的方法,对广西地区汉族53例PM/DM患者和汉族100例健康对照者进行HLA-DQA110个、-DQB15个等位基因分型。
     结果:1.HLA-DQA1等位基因频率分布
     PM/DM患者组中,检出10个等位基因,基因频率范围为0.057~0.340。其中,DQA1*0101、*0102、*0302等位基因频率较高(分别为0.340、0.255.0.226),DQA1*0201、*0501、*0601等位基因频率较低(分别为0.057、0.094、0.057)。对照组中,检出10个等位基因,基因频率范围为0.015~0.260。其中,DQA1*0101、*0102、*0104、*0302等位基因频率较高(分别为0.260、0.215、0.240),DQA1*0103、*0302、*0601等位基因频率较低(分别为0.065、0.015、0.035、0.060)。
     2.HLA-DQB1等位基因频率分布
     PM/DM患者组中,检出5个等位基因,基因频率范围为0.009~0.123。其中DQB1*0301等位基因的频率较高(为0.094),DQB1*0201、*0401频率较低(为0.047、0.019)。对照组中,检出4个等位基因,基因频率范围为0.000~0.095。其中DQB1*0301等位基因的频率较高(为0.085),DQB1*0501、*0601频率较低(分别为0.070、0.055)。
     3.HLA-DQA1、-DQB1等位基因频率比较
     PM/DM患者组与正常对照组比较,PM/DM患者组HLA-DQA1*0302、*0401等位基因频率呈显著增高,差异有显著性(OR值分别为26.759、5.244;P值分别为0.000、0.000,校正Pc值分别为0.000,0.004)。而等位基因HLA-DQA1*0201.*0501频率降低(OR值分别为0.328、0.413;P值分别为(0.018、0.028),但校正Pc>0.05,无统计学意义。
     4.伴间质性肺炎组HLA-DQA1、-DQB1等位基因分布
     4.1PM/DM伴间质性肺炎患者组中,HLA-DQA1检出9个等位基因,基因频率范围为0.026~0.395。其中DQA1*0102、*0104、*0401等位基因的频率较高(分别为0.211、0.237、0.237),DQA1*0103、*0501频率较低(分别为0.079、0.079),DQA1*0201未检出。
     4.2PM/DM伴间质性肺炎患者组中,HLA-DQB1检出5个等位基因,基因频率范围为0.026-0.132。其中DQB1*0201/、*0301等位基因的频率较高(分别为0.053、0.053),DQB1*0401、*0501频率较低(分别为0.026、0.026)。
     5.不伴间质性肺炎组HLA-DQA1、-DQB1等位基因分布
     5.1PM/DM不伴间质性肺炎患者组中,HLA-DQA1检出10个等位基因,基因频率范围为0.074~0.309。其中DQA1*0102、*0302等位基因的频率较高(分别为0.279、0.279),DQA1*0201、*0401频率较低(分别为0.088、0.088)。
     5.2PM/DM不伴间质性肺炎患者组中,HLA-DQB1检出4个等位基因,基因频率范围为0.015-0.118。其中DQB1*0301、*0601等位基因的频率较高(分别为0.118、0.118),DQB1*0201频率较低(为0.044),DQB1*0401未检出。
     6.伴间质性肺炎组和不伴间质性肺炎组HLA-DQA1、-DQB1等位基因分布比较
     PM/DM患者伴间质性肺炎组等位基因HLA-DQA1*0302、*401频率明显高于正常对照组(OR值分别为11.548、11.957;P值分别为0.003、0.000,校正Pc值分别为0.026、0.000)。与正常对照组比较,PM/DM患者不伴间质性肺炎组等位基因HLA-DQA1*0302频率明显增高(OR=40.956,P=0.000, Pc=0.000),而等位基因HLA-DQB1*0501频率呈降低趋势(P=0.021),但校正Pc>0.05,无统计学意义。
     结论:等位基因HLA-DQA1*0302、*0401可能是广西地区汉族PM/DM患者的易感基因。HLA-DQA1*0401可能是广西地区汉族PM/DM患者伴间质性肺炎的危险基因。
Objective:To investigate the genetic susceptibility of HLA-DQA1,-DQB1alleles to polymyositis/dermatomyositis in Chinese hans from guangxi area around.
     Methods:53patients with polymyositis/dermatomyositis and100healthy controls were examined for genotypes, HLA-DQA1,-DQB1allele typing was carried out using the polymerase reaction-sequence specific primers PCR (PCR-SSP).
     Results:1. HLA-DQA1allele frequency distribution
     PM/DM patients group were detected10alleles, the gene frequency range of0.057-0.340. Among them, the DQA1*0101,*0102,*0302allele frequency was higher (0.340,0.255,0.226), DQA1*0201,*0501,*0601allele frequency was lower (respectively0.057,0.094,0.057). Control group were detected10alleles in the gene frequency range of0.015to0.260. Among them, the DQA1*0101,*0102,*0104,*0302allele frequency was higher (0.260,0.215,0.240), DQA1*0103,*0302,*0601allele frequency was lower (0.065,0.015,0.035,0.060).
     2. HLA-DQB1allele frequencies
     PM/DM patients group were detected five alleles, the gene frequency range of0.009to0.123. DQB1*0301allele frequency was higher (0.094), DQB1*0201,*0401frequency is low (0.047,0.019). The control group, were detected in the4alleles, gene frequency range of0.000to0.095. DQB1*0301allele frequency was higher (0.085), DQB1*0501,*0601frequency is lower (0.070,0.055).
     3. HLA-DQA1,-DQB1alleles frequency
     PM/DM patients group and normal control group, the PM/DM patients group of HLA-DQA1*0302,*0401allele frequency was significantly increased, the difference was significant (OR values were26.759,5.244; P values were0.000correction Pc value were0.000,0.000,0.004). Alleles of HLA-DQA1*0201,*0501frequency is reduced (OR value to0.328,0.413;P values were0.018,0.028), but the correction to the Pc>0.05, not statistically significant.
     4. With interstitial pneumonia group, HLA-DQA1,-DQB1alleles distribution
     4.1PM/DM with interstitial pneumonia patient group, the HLA-DQA1were detected in9alleles, gene frequency range of0.026-0.395. DQA1*0102,*0104,*0401allele frequency was higher (0.211,0.237,0.237), DQA1*0103,*0501frequency was lower (0.079,0.079) of DQA1*0201is not seized out.
     4.2PM/DM with interstitial pneumonia patient group, the HLA-DQB1were detected five alleles, the gene frequency range of0.026-0.132. DQB1*0201,*0301allele frequency was higher (for the0.053,0.053), DQB1*0401,*0501frequency is lower (0.026,0.026).
     5. Without interstitial pneumonia group, HLA-DQA1,-DQB1alleles distribution
     5.1PM/DM without interstitial pneumonia patient group, the HLA-DQA1were detected in10alleles, gene frequency range from0.074to0.309, Which DQA1*0102,*0302allele frequency was higher (for the0.279,0.279), DQA1*0201,*0401frequency was lower (respectively, are0.088,0.088).
     5.2PM/DM without interstitial pneumonia patient group, the HLA-DQB1were detected in the4alleles, gene frequency range of0.015to0.118. DQB1*0301,*0601allele frequency was higher (for the0.118,0.118), DQB1*0201frequency was lower (0.044), DQB1*0401were not detected.
     6. With interstitial pneumonia group and without interstitial pneumonia group, HLA-DQA1,-DQB1alleles distribution
     PM/DM patients with interstitial pneumonia group alleles of HLA-DQA1*0302,*0401frequency was significantly higher than the heathy control group (OR=11.548,11.957; P values were0.003,0.000; correction Pc values were0.026,0.000). Compared with the normal control group, the PM/DM patients with interstitial pneumonia group of alleles of HLA-DQA1*0302frequency was significantly higher (OR=40.956, P=0.000, Pc=0.000), while the alleles of HLA-DQB1*0501frequency was decreased (P=0.021), but correction Pc>0.05, not statistically significant.
     Conclusion:Alleles of HLA-DQA1*0302,*0401have a significant genetic correlation with PM/DM, HLA-DQA1*0302,*0401with PM/DM were susceptibility genes in Guangxi Han patients with or without interstitial pneumonia may have different genetic immunological background. HLA-DQA1*0401may be dangerous gene of Han nationality in Guangxi region associated interstitial pneumonia in PM/DM patients.
引文
[1]Shamim EA, Rider LG, Pandey JP, et al. Differences in idiopathic inflammatory myopathy phenotypes and genotypes between Mesoamerican Mestizos and North American Caucasians: ethnogeographic influences in the genetics and clinical expression of myositis[J]. Arthritis Rheum,2002,46(7):1885-1893.
    [2]O'Hanlon TP, Carrick DM, Arnett FC, et al. Immunogenetic risk and protective factors for the idiopathic inflammatory myopathies:distinct HLA-A,-B,-Cw,-DRB1 and -DQA1 allelic profiles and motifs define clinicopathologic groups in caucasians[J]. Medicine,2005, 84(6):338-349.
    [3]Mamyrova G, O'Hanlon TP, Monroe JB, et al. Immunogenetic risk and protective factors for juvenile dermatomyositis in Caucasians[J]. Arthritis Rheum,2006,54(12):3979-3987.
    [4]Hausmanowa-Petrusewicz I, Kowalska-Oledzka E, Miller FW, et al. Clinical, serologic, and immunogenetic features in Polish patients with idiopathic inflammatory myopathies [J]. Arthritis Rheum,1997, 40(7):1257-1266.
    [5]Tomono N, Mori M, Nakajima S, et al. HLA-DRB1*15021 is the predominant allele in Japanese patients with juvenile dermatomyositis[J]. J Rheumatol,2004,31(9):1847-1850.
    [6]Furuya T, Hakoda M, Tsuchiya N, et al. Immunogenetic features in 120 Japanese patients with idiopathic inflammatory myopathy [J]. Rheumatol, 2004,31(9):1768-1774.
    [7]韩秀萍,翟宁,耿龙.]KLA-Ⅱ类基因单倍型与中国北方汉族人皮肌炎/多发性肌炎的相关性研究[J].中国免疫学杂志,2004,20(2):198-212.
    [8]臧松,邓学新,甘晓丹,等.HLA-DR2, DRB1-*0301, DQA1-*0501基因频率与肌炎及其临床表现的相关性分析[J].中华风湿病学杂志,1998,2(4):208-210.
    [9]赵辨.中国临床皮肤病学.第1版[M].江苏:江苏科学技术出版社,2009,813.
    [10]Demedts M, Costabel U. ATS/ERS international multidisciplinary consensus classification of the idiopathic interstitial pneumonias[J]. European Respiratory Journal,2002,19(5):794-796.
    [11]Bunce M, Taylor CJ, Welsh KI. Rapid HLA-DQB typing by eight polymerase chain reaction amplifications with sequence-specific primers (PCR-SSP)[J]. Human immunology,1993,37(4):201-206.
    [12]龙桂芳,阿卜迪.应用序列特异引物PCR法对广西壮族HLA-DQA1进行基因分型[J]冲华血液学杂志,1995,16(10):532-534.
    [13]Scharf S, Saiki R, Erlich. H, et.al. New methodology for HLA classⅡ. Human Immunal[J],1988,27(7):23-143.
    [14]戚豫,唐炬.DNA单链构象多态性原理初探[J].基础医学与临床,1997,17(2):142-146.
    [15]龚非力,医学免疫学.第3版[M].北京:科学技术出版社,2009:92-94.
    [16]van der Woude D, Lie BA, Lundstrom E, et al. Protection against anti-citrullinated protein antibody-positive rheumatoid arthritis is predominantly associated with HLA-DRB 1*1301:A meta-analysis of HLA-DRB 1 associations with anti-citrullinated protein antibody-positive and anti-citrullinated protein antibody-negative rheumatoid arthritis in four European populations [J]. Arthritis & Rheumatism,2010, 62(5):1236-1245.
    [17]Terao C, Ohmura K, Kochi Y, et al. A large-scale association study identified multiple HLA-DRB1 alleles associated with ACPA-negative rheumatoid arthritis in Japanese subjects[J]. Annals of the rheumatic diseases,2011,70(12):2134-2139.
    [18]谭立明,阙秋华,彭卫华.江西汉族人群类风湿关节炎易感性与HLA-DR基因相关性研究[J].免疫学杂志,2009,26(6):555-556.
    [19]徐金瑞,张东涛,杨易,等.宁夏回族人群HLA-DQB1基因多态性与类风湿性关节炎的相关性[J].陕西医学杂志,2009,(3):295-297.
    [20]蒋真,李向培,钱龙,等.HLA-DRB1等位基因分型与类风湿关节炎相关性研究[J].安徽医药,2010,14(11):1299-1302.
    [21]Rezaieyazdi Z, Tavakkol-Afshari J, Esmaili E, et al. Association of HLA-DQB1 allelic sequence variation with susceptibility to systemic lupus erythematosus[J]. Iranian Journal of Allergy, Asthma and Immunology,2008,7(2):221-229.
    [22]Castano-Rodriguez N, Diaz-Gallo LM, Pineda-Tamayo R, et al. Meta-analysis of HLA-DRB1 and HLA-DQB1 polymorphisms in Latin American patients with systemic lupus erythematosus[J]. Autoimmunity reviews,2008,7(4):322-330.
    [23]Cowland JB, Andersen V, Halberg P, et al. DNA polymorphism of HLA class II genes in systemic lupus erythematosus[J]. Tissue Antigens,1994, 43(1):34-37.
    [24]孙静,巫志峰,韩凌.HLA-DQB1等位基因与广东汉族人群系统性红斑狼疮相关性研究[J].中国实用医药,2009,4(2):62-63.
    [25]陈跃华,陈明,范昌斌.中国汉族人群系统性红斑狼疮HLA-DQ基因多态性的Meta分析[J].安徽医药,2006,10(6):447-449.
    [26]刘栋华,梁伶,苏家光,等.广西壮族系统性红斑狼疮自身抗体与HLA-DQA1等位基因的相关性[J].广西医科大学学报,2007,24(2):186-188.
    [27]Simeon CP, Fonollosa V, Tolosa C, et al. Association of HLA class Ⅱ genes with systemic sclerosis in Spanish patients[J]. The Journal of Rheumatology,2009,36(12):2733-2736.
    [28]Favalli E, Ingegnoli F, Zeni S, Fare M,Fantini F. HLA typing in systemic sclerosis[J]. Reumatismo,2011,53(3):210-214.
    [29]朱薇,严煜林.HLA-DRB1与广西地区系统性硬皮病的相关性研究[J].中华皮肤科杂志,2009,42(7):488-489.
    [30]周茂松,严煜林,罗虹.广西壮族系统性硬皮病与HLA-DRB1等位基因关联性研究[J].中华风湿病学杂志,2011,15(1):34-37.
    [31]韩福海,严煜林.广西壮族汉族系统性硬化病与HLA-DQA1、DQB1等位基因相关性研究[J].中华皮肤科杂志,2011,44(4):235-237.
    [32]王岩,赵玉铭,宋芳吉.北方汉族寻常型银屑病与HLA等位基因的关联研究[J].中国麻风皮肤病杂志,2006,22(1):1-4.
    [33]张学军,魏生才HLA-DQA1及DQB1等位基因与寻常型银屑病遗传易感性研究[J].中华皮肤科杂志,2002,35(2):120-123.
    [34]李维,吴强HLA-B27亚型及其与强直性脊柱炎关系的研究进展[J].免疫学杂志,2002,18(6):191-194.
    [35]O'Donnell B, O'neill C, Francis D, et al. Huma leucocyte antigen class II associations in chronic idiopathic urticaria[J]. British Journal of Dermatology,1999,140(5):853-858.
    [36]蒙金秋,吴易,何钠,等.广西壮族慢性荨麻疹患者与HLA-DRB1基因的相关性[J].广西医科大学学报,2010,27(6):875-877.
    [37]谭志建,陈静,李家文,熊平.慢性荨麻疹与HLA-DRB1,DQB1基因的相 关性研究[J].中国麻风皮肤病杂志,2006,22(5):369-371.
    [38]Horiki T, Ichikawa Y, Moriuchi J, et al. HLA class Ⅱ haplotypes associated with pulmonary interstitial lesions of polymyositis and dermatomyositis in Japanese patients[J]. Tissue Antigens,2002, 59(1):25-30.
    [39]Fathi M, Lundberg IE. Interstitial lung disease in polymyositis and dermatomyositis[J]. Current opinion in rheumatology,2005,17(6):701.
    [40]Stanevicha V, Eglite J, Zavadska D, et al. HLA class Ⅱ DR and DQ genotypes and haplotypes associated with rheumatic fever among a clinically homogeneous patient population of Latvian children[J]. Arthritis Research and Therapy,2007,9(3):58.
    [1]赵辨.中国临床皮肤病学.第1版[M].江苏:江苏科学技术出版社,2009.
    [2]王国春.对特发性炎性肌病诊断标准的新认识[J].中华风湿病学杂志,2009,12(4):219-221.
    [3]刘鹏.多发性肌炎的研究进展[J].海军总医院学报,2008,21(2):103-105.
    [4]Chinoy H, Lamb JA, Ollier WE, et al. An update on the immunogenetics of idiopathic inflammatory myopathies:major histocompatibility complex and beyond[J]. Current opinion in rheumatology,2009, 21(6):588-593.
    [5]Tomono N, Mori M, Nakajima S, et al. HLA-DRB1*1502 is the predominant allele in Japanese patients with juvenile dermatomyositis[J]. The Journal of Rheumatology,2004,31(9):1847.
    [6]边红,焉传祝.多发性肌炎/皮肌炎免疫发病机制研究进展[J].国际神经病学神经外科学杂志,2006,33(1):86-87.
    [7]王培珍,管剑龙,韩星海.特发性炎性肌病的免疫学研究进展[J].第二军医大学学报,2008,29(4):443-445.
    [8]龚非力.医学免疫学.第3版[M].北京:科学技术出版社,2009.
    [9]张开明.最新皮肤科学理论与实践[M].北京:中国医药科技出版社,2011,445.
    [10]Pachman LM, Jonasson O, Cannon RA, et al. HLA-B8 in juvenile dermatomyositis[J]. Lancet,1977,2(8037):567-568.
    [11]Hirsch TJ, Enlow RW, Bias WB, et al. HLA-D related (DR) antigens in various kinds of myositis[J]. Hum Immunol,1981,3(2):181-186.
    [12]Friedman JM, Pachman LM, Maryjowski ML, et al. Immunogenetic studies of juvenile dermatomyositis. HLA antigens in patients and their families[J]. Tissue Antigens,1983,21(1):45-49.
    [13]Pachman LM, Maryjowski MC. Juvenile dermatomyositis and polymyositis[J].Clin Rheum Dis,1984,10(1):95-115.
    [14]Carroll GJ, Will RK, Peter JB, et al. Penicillamine induced polymyositis and dermatomyositis[J]. Rheumatol,1987,14(5):995-1001.
    [15]Robb SA, Fielder AH, Saunders CE, et al. C4 complement allotypes in juvenile dermatomyositis[J]. Hum Immunol,1988,22(1):31-38.
    [16]Goldstein R, Duvic M, Targoff IN, et al. HLA-D region genes associated with autoantibody responses to histidyl-transfer RNA synthetase (Jo-1) and other translation-related factors in myositis[J]. Arthritis Rheum,1990, 33(8):1240-1248.
    [17]Reed AM, Pachman L,Ober C. Molecular genetic studies of major histocompatibility complex genes in children with juvenile dermatomyositis:increased risk associated with HLA-DQA1*0501[J]. Hum Immunol,1991,32(4):235-240.
    [18]Ehrenstein MR, Snaith ML, Isenberg DA. Idiopathic myositis:a rheumatological view[J]. Ann Rheum Dis,1992,51(1):41-44.
    [19]Garlepp MJ. Immunogenetics of inflammatory myopathies[J]. Baillieres ClinNeurol,1993,2(3):579-597.
    [20]Reed AM, Stirling JD. Association of the HLA-DQAl*0501 allele in multiple racial groups with juvenile dermatomyositis [J]. Hum Immunol, 1995,44(3):131-135.
    [21]Arnett FC, Targoff IN, Mimori T, et al. Interrelationship of major histocompatibility complex class II alleles and autoantibodies in four ethnic groups with various forms of myositis[J]. Arthritis Rheum,1996, 39(9):1507-1518.
    [22]Furuya T, Hakoda M, Higami K, et al. Association of HLA class I and class II alleles with myositis in Japanese patients[J]. J Rheumatol,1998, 25(6):1109-1114.
    [23]Rider LG, Shamim E, Okada S, et al. Genetic risk and protective factors for idiopathic inflammatory myopathy in Koreans and American whites:a tale of two loci[J]. Arthritis Rheum,1999,42(6):1285-1290.
    [24]Shamim EA, Rider LG, Pandey JP, et al. Differences in idiopathic inflammatory myopathy phenotypes and genotypes between Mesoamerican Mestizos and North American Caucasians: ethnogeographic influences in the genetics and clinical expression of myositis[J]. Arthritis Rheum,2002,46(7):1885-1893.
    [25]Horiki T, Ichikawa Y, Moriuchi J, et al. HLA class II haplotypes associated with pulmonary interstitial lesions of polymyositis/dermatomyositis in Japanese patients[J]. Tissue Antigens, 2002,59(1):25-30.
    [26]O'Hanlon T, Carrick D, Targoff I, et al. Immunogenetic risk and protective factors for the idiopathic inflammatory myopathies:distinct HLA-A,-B,-Cw,-DRB1, and-DQAl allelic profiles distinguish European American patients with different myositis autoantibodies[J]. Medicine, 2006,85(2):111.
    [27]Mamyrova G, O'Hanlon TP, Monroe JB, et al. Immunogenetic risk and protective factors for juvenile dermatomyositis in Caucasians [J]. Arthritis Rheum,2006,54(12):3979-3987.
    [28]Scott AP, Allcock RJ, Mastaglia F, et al. Sporadic inclusion body myositis in Japanese is associated with the MHC ancestral haplotype 52.1 [J]. Neuromuscul Disord,2006,16(5):311-315.
    [29]Wedderburn L, McHugh N, Chinoy H, et al. HLA class II haplotype and autoantibody associations in children with juvenile dermatomyositis and juvenile dermatomyositis scleroderma overlap[J]. Rheumatology,2007, 46(12):1786.
    [30]Chinoy H, Payne D, Poulton KV, et al. HLA-DPB1 associations differ between DRB1*03 positive anti-Jo-1 and anti-PM-Scl antibody positive idiopathic inflammatory myopathy[J]. Rheumatology (Oxford),2009, 48(10):1213-1217.
    [31]臧松,邓学新,甘晓丹,等.HLA-DR2,DRB1-*0301,DQA1-*0501基因频率与肌炎及其临床表现的相关性分析[J].中华风湿病学杂志,1998,2(4):208-210.
    [32]韩秀萍,翟宁,张庆瑞,等.HLA-DQB等位基因与皮肌炎/多发性肌炎相关性研究[J].中华医学遗传学杂志,2002,(4):56-57.
    [33]韩秀萍,翟宁,张英志,等.HLA-DRB1等位基因与中国北方汉族多发性肌炎皮肌炎的相关性[J].中华微生物学和免疫学杂志,2003,(3):69-71.
    [34]韩秀萍,翟宁,耿龙,等.HLA-Ⅱ类基因单倍型与中国北方汉族人皮肌炎多发性肌炎的相关性研究[J].中国免疫学杂志,2004,(9):614-616.
    [35]O'Hanlon TP, Carrick DM, Arnett FC, et al. Immunogenetic risk and protective factors for the idiopathic inflammatory myopathies:distinct HLA-A,-B,-Cw,-DRB1 and-DQA1 allelic profiles and motifs define clinicopathologic groups in caucasians[J]. Medicine,2005, 84(6):338-349.
    [36]O'Hanlon TP, Miller FW. Genetic risk and protective factors for the idiopathic inflammatory myopathies[J]. Current rheumatology 2009, 11(4):287-294.
    [37]Chinoy H, Salway F, John S, et al. Tumour necrosis factor-a single nucleotide polymorphisms are not independent of HLA class I in UK Caucasians with adult onset idiopathic inflammatory myopathies[J]. Rheumatology,2007,46(9):1411.
    [38]Mastaglia FL, Needham M, Scott A, et al. Sporadic inclusion body myositis:HLA-DRB1 allele interactions influence disease risk and clinical phenotype[J]. Neuromuscular Disorders,2009,19(11):763-765.
    [39]Connors GR, Christopher-Stine L, Oddis CV, et al. Interstitial lung disease associated with the idiopathic inflammatory myopathies:what progress has been made in the past 35 years[J]. Chest,2010,138(6):1464.
    [40]Furuya T, Hakoda M, Tsuchiya N, et al. Immunogenetic features in 120 Japanese patients with idiopathic inflammatory myopathy[J]. Rheumatol, 2004,31(9):1768-1774.
    [41]Tomono N, Mori M, Nakajima S, et al. HLA-DRB 1*1502 is the predominant allele in Japanese patients with juvenile dermatomyositis[J]. Rheumatol,2004,31(9):1847-1850.
    [42]Betteridge ZE, Gunawardena H, McHugh NJ. Novel autoantibodies and clinical phenotypes in adult and juvenile myositis[J]. Arthritis Res Ther, 2011,13(2):209.
    [43]Khanna S, Reed AM. Immunopathogenesis of juvenile dermatomyositis[J]. Muscle & nerve,2010,41(5):581-592.
    [44]Gunawardena H, Wedderburn L, Chinoy H, et al. Autoantibodies to a 140-kd protein in juvenile dermatomyositis are associated with calcinosis[J]. Arthritis & Rheumatism,2009,60(6):1807-1814.
    [45]O'Hanlon TP, Carrick DM, Targoff IN, et al. Immunogenetic risk and protective factors for the idiopathic inflammatory myopathies:distinct HLA-A,-B,-Cw,-DRB1, and -DQAl allelic profiles distinguish European American patients with different myositis autoantibodies[J]. Medicine (Baltimore),2006,85(2):111-127.
    [46]O'Hanlon TP, Rider LG, Mamyrova G, et al. HLA polymorphisms in African Americans with idiopathic inflammatory myopathy:allelic profiles distinguish patients with different clinical phenotypes and myositis autoantibodies[J]. Arthritis Rheum,2006,54(11):3670-3681.
    [47]Wedderburn LR, McHugh NJ, Chinoy H, et al. HLA class Ⅱ haplotype and autoantibody associations in children with juvenile dermatomyositis and juvenile dermatomyositis-scleroderma overlap[J]. Rheumatology, 2007,46(12):1786-1791.
    [48]Betteridge Z, Gunawardena H, Chinoy H, et al. Clinical and human leucocyte antigen class Ⅱ haplotype associations of autoantibodies to small ubiquitin-like modifier enzyme, a dermatomyositis-specific autoantigen target, in UK Caucasian adult-onset myositis[J]. Annals of the rheumatic diseases,2009,68(10):1621.
    [49]Hausmanowa-Petrusewicz I, Kowalska-Oledzka E, Miller FW, et al. Clinical, serologic, and immunogenetic features in Polish patients with idiopathic inflammatory myopathies[J]. Arthritis Rheum,1997, 40(7):1257-1266.

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