医学
免疫学
内科学
分子模拟
类风湿性关节炎
免疫衰老
人口
病毒学
自身免疫
疾病
免疫系统
环境卫生
作者
Yen‐Tze Liu,Hsi‐Kai Tsou,Jeng‐Yuan Chiou,Yu‐Hsun Wang,Ming-Chih Chou,James Cheng‐Chung Wei
标识
DOI:10.1136/annrheumdis-2019-215931
摘要
Rheumatoid arthritis (RA) is an autoimmune disease caused by genetic and environmental factors. Infection is proposed to contribute to the pathogenesis.1 Several viral and bacterial infections, including parvovirus B19, Chikungunya, hepatitis C, Epstein-Barr virus and Porphyromonas gingivalis , have been raised to be associated with RA.1 The mechanism of how infections affect RA remains undetermined, generally considered to be via molecular mimicry and cross-reactions between self-antigens and viral proteins.1 Furthermore, recent study postulates that RA may be the result of immunosenescence, meaning premature ageing of the immune system via various mechanisms including telomere shortening.2 A recent review article illustrates that the expression of human telomerase reverse transcriptase was influenced by human papillomavirus (HPV) E6/E7.3 Therefore, immunosenescence caused by telomere shortening may be another hypothetical mechanism in RA development followed by HPV infection.
HPV infections have been found to be associated with autoimmune diseases including systemic lupus erythematosus and RA.4 5 …
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