Maldonado Anastacia, Mueller Yvonne M, Thomas Preethi, Bojczuk Paul, O'Connors Carolyn, Katsikis Peter D
Department of Medicine, Drexel University College of Medicine, Drexel University, Philadelphia, Pennsylvania, USA.
Arthritis Res Ther. 2003;5(2):R91-6. doi: 10.1186/ar619. Epub 2003 Jan 6.
Although a role for CD8+ T cells in the pathogenesis of rheumatoid arthritis (RA) has been suggested, the precise nature of their involvement is not fully understood. In the present study we examined the central and effector memory phenotypes of CD4+ and CD8+ T cells in the peripheral blood of patients with RA and systemic lupus erythematosus. Terminally differentiated effector memory CD45RA+CD62L-CD8+ T cells were significantly decreased in RA patients, whereas the central memory CD45RA-CD62L+ CD8+ T-cell population was increased as compared with levels in healthy control individuals. Naïve and preterminally differentiated effector memory CD45RA-CD62L- CD8+ T cells did not differ between RA patients and control individuals. The CD45RA-CD62L+ central memory CD4+ T-cell subpopulation was increased in RA patients, whereas the naïve and effector memory phenotype of CD4+ T cells did not differ between RA patients and control individuals. In patients with systemic lupus erythematosus the distribution of naïve/memory CD4+ and CD8+ T cells did not differ from that in age- and sex-matched control individuals. These findings show that peripheral blood CD8+ T cells from RA patients exhibit a skewed maturation phenotype that suggests a perturbation in the homeostasis of these cells. The central memory CD45RA-CD62L+ CD4+ and CD8+ T-cell numbers were increased in RA, suggesting an accelerated maturation of naïve T cells. The decreased numbers of terminally differentiated CD45RA+CD62L- effector memory CD8+ T cells in peripheral blood of RA patients may reflect increased apoptosis of these cells or enhanced migration of these cells to sites of inflammation, which may play a role in the pathogenesis of RA.
虽然已有研究提示CD8 + T细胞在类风湿关节炎（RA）发病机制中发挥作用，但其具体参与机制尚未完全明确。在本研究中，我们检测了RA和系统性红斑狼疮患者外周血中CD4 +和CD8 + T细胞的中枢记忆和效应记忆表型。与健康对照个体相比，RA患者终末分化的效应记忆CD45RA + CD62L - CD8 + T细胞显著减少，而中枢记忆CD45RA - CD62L + CD8 + T细胞群体增加。RA患者和对照个体之间，初始及终末分化前的效应记忆CD45RA - CD62L - CD8 + T细胞无差异。RA患者中CD45RA - CD62L +中枢记忆CD4 + T细胞亚群增加，而RA患者和对照个体之间CD4 + T细胞的初始和效应记忆表型无差异。在系统性红斑狼疮患者中，初始/记忆CD4 +和CD8 + T细胞的分布与年龄和性别匹配的对照个体无差异。这些结果表明，RA患者外周血CD8 + T细胞表现出成熟表型的偏态分布，提示这些细胞的稳态受到干扰。RA患者中中枢记忆CD45RA - CD62L + CD4 +和CD8 + T细胞数量增加，提示初始T细胞成熟加速。RA患者外周血终末分化的CD45RA + CD62L -效应记忆CD8 + T细胞数量减少，可能反映了这些细胞凋亡增加或向炎症部位迁移增强，这可能在RA发病机制中起作用。
