Presentation of self peptides by dendritic cells: possible implications for the pathogenesis of rheumatoid arthritis.
Presentation of self peptides by dendritic cells: possible implications for the pathogenesis of rheumatoid arthritis.
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DOI：
10.1002/art.1780390202
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发表时间：
1996-02
影响因子：
--
通讯作者：
Ranjeny Thomas;P. Lipsky
中科院分区：
文献类型：
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作者：
Ranjeny Thomas;P. Lipsky
类风湿性关节炎（RA）可能是炎症部位和全身因素复杂相互作用的结果。尽管人们对 RA 的发病过程了解很多，但引发或驱动该疾病的致关节炎抗原尚不清楚。一种或多种外源抗原可能是造成这种情况的原因，但尚未证实有令人信服的外源候选抗原。此外，RA 没有发生“流行病”，而且 RA 不能通过血液或器官输血传播，这表明传染源并不是其发病的直接原因。对 RA 中树突状细胞 (DC) 的研究表明，另一种假设是，内源性抗原激活 T 细胞可能足以引发该疾病。
Rheumatoid arthritis (RA) likely results from a complex interplay of factors both at the site of inflammation and systemically. Although much is known about the pathogenetic processes that occur in RA, the arthritogenic antigen (s) that initiate or drive the disease are not known. One or a number of exogenous antigens may be responsible, but no convincing exogenous candidate antigen has yet been demonstrated. Furthermore, the lack of occurrence of “epidemics” of RA and the fact that RA cannot be transferred by blood or organ transfusion suggests that an infectious agent is not directly responsible for its onset. An alternative hypothesis, suggested by the study of dendritic cells (DC) in RA, is that activation of T cells by endogenous antigens might be sufficient to drive the disease.