Nardelli Dean T, Warner Thomas F, Callister Steven M, Schell Ronald F
University of Wisconsin, Wisconsin State Laboratory of Hygiene, 465 Henry Mall, Madison, WI 53706, USA.
Clin Vaccine Immunol. 2006 Aug;13(8):884-91. doi: 10.1128/CVI.00137-06.
CD4(+) CD25(+) T cells are a population of regulatory T cells responsible for the modulation of the immune response in several autoimmune and infectious disease models. We previously showed that adoptive transfer of enriched CD4(+) CD25(+) T cells also plays a major role in the prevention of arthritis in Borrelia-vaccinated (Borrelia burgdorferi isolate 297) and -challenged (B. bissettii) mice. Here, we present evidence that administration of anti-CD25 antibody at the time of challenge or at later intervals fails to enhance the development of severe destructive osteoarthropathy in Borrelia-vaccinated C57BL mice. However, Borrelia-vaccinated and -challenged mice receiving anti-CD25 antibody developed decreased borreliacidal antibody titers compared to vaccinated and challenged controls. These findings suggest that additional mechanisms besides CD4(+) CD25(+) T cells are involved in the regulation of the immune response to Borrelia infection following vaccination.
CD4(+)CD25(+)T细胞是一群调节性T细胞，在多种自身免疫性疾病和感染性疾病模型中负责调节免疫反应。我们之前表明，富集的CD4(+)CD25(+)T细胞的过继转移在预防接种伯氏疏螺旋体疫苗（伯氏疏螺旋体分离株297）并受到攻击（比氏疏螺旋体）的小鼠发生关节炎中也起主要作用。在此，我们提供证据表明，在攻击时或之后的时间段给予抗CD25抗体并不能增强接种伯氏疏螺旋体疫苗的C57BL小鼠严重破坏性骨关节炎的发展。然而，与接种疫苗并受到攻击的对照相比，接受抗CD25抗体的接种伯氏疏螺旋体疫苗并受到攻击的小鼠产生的杀伯氏疏螺旋体抗体滴度降低。这些发现表明，除了CD4(+)CD25(+)T细胞外，其他机制也参与了接种疫苗后对伯氏疏螺旋体感染的免疫反应调节。
