Buckley Christopher D
Department of Rheumatology, City Hospital NHS Trust, University of Birmingham.
Clin Med (Lond). 2003 Jul-Aug;3(4):361-6. doi: 10.7861/clinmedicine.3-4-361.
Inflammation is a beneficial host response to tissue damage. Most episodes of inflammation resolve spontaneously and do not persist. However, in rheumatoid arthritis (RA), as in a number of other chronic inflammatory diseases, the inflammatory response persists and a stable inflammatory infiltrate accumulates in the joint. What drives this persistence and the relative contribution of infiltrating leucocytes and stromal cells such as fibroblasts to the stability of the inflammatory process are the subject of this article. Fibroblasts play an important role in defining the disordered synovial microenvironment in RA. Through their production of a variety of cytokines and constitutive chemokines they directly alter the behaviour of infiltrating leucocytes, leading to their inappropriate survival and retention. These findings suggest that stromal cells such as fibroblasts play an important role in the switch from acute resolving to chronic persistent arthritis by allowing lymphocytes to accumulate in the wrong place at the wrong time.
炎症是机体对组织损伤的一种有益反应。大多数炎症发作会自发消退，不会持续存在。然而，类风湿关节炎（RA）与其他一些慢性炎症性疾病一样，炎症反应持续存在，关节内会积累稳定的炎症浸润。是什么驱动了这种持续性以及浸润的白细胞和成纤维细胞等基质细胞对炎症过程稳定性的相对贡献是本文的主题。成纤维细胞在界定类风湿关节炎中紊乱的滑膜微环境方面发挥着重要作用。通过产生多种细胞因子和组成性趋化因子，它们直接改变浸润白细胞的行为，导致其异常存活和滞留。这些发现表明，成纤维细胞等基质细胞通过使淋巴细胞在错误的时间积聚在错误的位置，在从急性消退性关节炎向慢性持续性关节炎的转变中起重要作用。
