Smolen J S, Tohidast-Akrad M, Gal A, Kunaver M, Eberl G, Zenz P, Falus A, Steiner G
2nd Department of Medicine, Lainz Hospital, Vienna, Austria.
Scand J Rheumatol. 1996;25(1):1-4. doi: 10.3109/03009749609082660.
In this review the involvement of T cells, in addition to that of the monocyte/macrophage lineage, in the pathogenesis of rheumatoid arthritis is discussed. The evidence for the pathogenetic importance of T cells is based upon their state of activation in the synovial membrane and the cytokines produced. These cytokines can be detected in synovial fluids as well as in the synovial membrane by both immunohistochemistry and in situ hybridization. However, cytokine production can be detected only in a minor fraction of the T cells which contrasts the number of non-T cells observed to synthesize cytokines. Nevertheless, it can be assumed that the small amount of lymphokines is sufficient to activate a cytokine cascade derived from other cells. The cytokine profile secreted is indicative for a T cell response that primarily involves Th1-like cells.
在本综述中，除了单核细胞/巨噬细胞系外，还讨论了T细胞在类风湿性关节炎发病机制中的作用。T细胞在发病机制中的重要性证据基于它们在滑膜中的激活状态以及产生的细胞因子。通过免疫组织化学和原位杂交技术，这些细胞因子可在滑液以及滑膜中检测到。然而，只能在一小部分T细胞中检测到细胞因子的产生，这与观察到的合成细胞因子的非T细胞数量形成对比。尽管如此，可以假定少量的淋巴细胞因子足以激活源自其他细胞的细胞因子级联反应。所分泌的细胞因子谱表明主要涉及Th1样细胞的T细胞反应。
