Kunkel S L, Lukacs N, Kasama T, Strieter R M
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602, USA.
J Leukoc Biol. 1996 Jan;59(1):6-12. doi: 10.1002/jlb.59.1.6.
Rheumatoid arthritis (RA) is an autoimmune disease characterized by the elicitation and activation of a number of leukocyte populations within both the synovial space and joint tissue. The recruited leukocytes subsequently play an instrumental role in synovial cell proliferation, pannus formation, and bone erosion. Although it is know that leukocytes are important participants in the evolving joint pathology, the mechanism responsible for the successful elicitation of cells to the joint is not clear. A number of studies have identified an association of specific cytokines, including chemokines, with active arthritis, but longitudinal analyses of cytokine expression and the causal role of these mediators have not been defined. Animal models and cell culture systems have proved useful in identifying the expression of various cytokines during the maintenance of chronic joint inflammation. In addition, animal models have provided important information regarding the kinetic production and contribution of specific mediators to the development of experimental arthritis. These studies provide insights into the potential mechanisms for leukocyte involvement in inflammatory joint disease.
类风湿性关节炎(RA)是一种自身免疫性疾病,其特征是滑膜间隙和关节组织内多种白细胞群体被募集和激活。随后,募集到的白细胞在滑膜细胞增殖、血管翳形成和骨质侵蚀中发挥重要作用。虽然已知白细胞是关节病变发展过程中的重要参与者,但负责成功将细胞募集到关节的机制尚不清楚。多项研究已确定特定细胞因子(包括趋化因子)与活动性关节炎有关,但尚未对细胞因子表达进行纵向分析,也未明确这些介质的因果作用。动物模型和细胞培养系统已被证明有助于确定慢性关节炎症维持期间各种细胞因子的表达。此外,动物模型还提供了有关特定介质的动力学产生及其对实验性关节炎发展的作用的重要信息。这些研究为白细胞参与炎性关节疾病的潜在机制提供了见解。