Jung Sundo, Shin Hyun-Suk, Hong Changwan, Lee Hyunji, Park Yoon-Kyung, Shin Jung Hoon, Hong Seokmann, Lee Gap Ryol, Park Se-Ho
School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, South Korea.
Biochem Biophys Res Commun. 2009 Dec 18;390(3):399-403. doi: 10.1016/j.bbrc.2009.09.008. Epub 2009 Sep 6.
The role of NKT cells in the pathogenesis of collagen-induced arthritis (CIA) remains unclear since most studies have used C57BL/6 (B6) mice, which are less susceptible to CIA than mice with a DBA/1 background. To clarify the immunological functions of NKT cells in CIA, it is necessary to analyze in detail the effects of NKT cell deficiency on CIA development in DBA/1 mice. The incidence and severity of CIA were significantly exacerbated in DBA/1CD1d(+/-) mice as compared to DBA/1CD1d(-/-) mice. In DBA/1CD1d(+/-) mice, antigen-specific responses of B and T cells against CII were remarkably increased and inflammatory cytokine levels were also increased in vivo and in vitro. The number of IL-17-producing NKT cells significantly increased in DBA/1CD1d(+/-) mice as the disease progressed. Our results clearly show that NKT cells are involved not only in accelerating the severity and incidence of CIA but also in perpetuating the disease progression.
自然杀伤T细胞（NKT细胞）在胶原诱导性关节炎（CIA）发病机制中的作用仍不清楚，因为大多数研究使用的是C57BL/6（B6）小鼠，与具有DBA/1背景的小鼠相比，它们对CIA的易感性较低。为了阐明NKT细胞在CIA中的免疫功能，有必要详细分析NKT细胞缺陷对DBA/1小鼠CIA发展的影响。与DBA/1CD1d（-/-）小鼠相比，DBA/1CD1d（+/-）小鼠中CIA的发病率和严重程度显著加剧。在DBA/1CD1d（+/-）小鼠中，B细胞和T细胞针对II型胶原（CII）的抗原特异性反应显著增加，体内和体外的炎性细胞因子水平也升高。随着疾病进展，DBA/1CD1d（+/-）小鼠中产生白细胞介素-17的NKT细胞数量显著增加。我们的结果清楚地表明，NKT细胞不仅参与加速CIA的严重程度和发病率，还参与使疾病进展持续下去。
