Polymyositis and Dermatomyositis: Pathophysiology

被引：34
作者：
Nagaraju, Kanneboyina [2 ,3 ]
Lundberg, Ingrid E. [1 ]
机构：
[1] Karolinska Inst, Dept Med, Rheumatol Unit, Karolinska Univ Hosp, SE-17176 Stockholm, Sweden
[2] Childrens Natl Med Ctr, Med Genet Res Ctr, Washington, DC 20010 USA
[3] George Washington Univ, Dept Integrat Syst Biol, Med Ctr, Washington, DC 20010 USA
来源：
RHEUMATIC DISEASE CLINICS OF NORTH AMERICA | 2011年 / 37卷 / 02期
基金：
美国国家卫生研究院; 瑞典研究理事会;
关键词：
Polymyositis; Dermatomyositis; Pathogenesis; Adaptive; Innate and nonimmune pathways; Skeletal muscle cell death; Autophagy and endoplasmic reticulum stress; MHC CLASS-I; IDIOPATHIC INFLAMMATORY MYOPATHIES; MYOSITIS-SPECIFIC AUTOANTIBODIES; ENDOPLASMIC-RETICULUM STRESS; INCLUSION-BODY MYOSITIS; TRANSFER-RNA-SYNTHETASE; INTERCELLULAR-ADHESION MOLECULE-1; INTERFERON-ALPHA TREATMENT; UNFOLDED PROTEIN RESPONSE; SKELETAL-MUSCLE LEADS;
D O I：
10.1016/j.rdc.2011.01.002
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Recent advances have increased the understanding of the pathogenesis of polymyositis and dermatomyositis. Clearly, the pathogenesis is complex, and adaptive (eg, autoimmune) and innate and nonimmune pathways play a role in the disease mechanisms, but the relative contribution may vary between patients and in different phases of the disease. Phenotyping patients using autoantibody profiling has resulted in information on molecular pathways that may be relevant in certain subsets of patients with polymyositis or dermatomyositis, but combining the autoantibody profiles with molecular signatures of innate and nonimmune mechanisms would enhance our ability to classify, diagnose, and treat these disorders more effectively.
引用
收藏
页码：159 / +
页数：14
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