Munson Erik L, DeCoster David J, Nardelli Dean T, England Douglas M, Callister Steven M, Schell Ronald F
Wisconsin State Laboratory of Hygiene, University of Wisconsin, Madison, Wisconsin 53706, USA.
Clin Diagn Lab Immunol. 2004 Jan;11(1):35-41. doi: 10.1128/cdli.11.1.35-41.2004.
Development of a high level of sustained borreliacidal antibody is paramount for maintaining protection against infection with Borrelia burgdorferi. We show that production of borreliacidal antibody can be enhanced by preventing the effects of gamma interferon (IFN-gamma). When lymph node cells capable of producing borreliacidal antibody were cultured with anti-murine IFN-gamma, an eightfold increase in borreliacidal antibody production was obtained. However, anti-IFN-gamma treatment of these cells also enhanced their ability to adaptively induce arthritis. When anti-IFN-gamma-treated lymph node cells producing borreliacidal antibody were infused into C3H/HeJ mice and the mice were then challenged with B. burgdorferi, the mice developed severe destructive Lyme arthritis. Additional studies are needed to delineate the immune response responsible for the induction of arthritis and production of borreliacidal antibody. These studies are needed to ensure an effective and safe vaccine against infection with B. burgdorferi.
产生高水平的持续性杀疏螺旋体抗体对于维持针对伯氏疏螺旋体感染的保护作用至关重要。我们发现,通过阻止γ干扰素(IFN-γ)的作用,可以增强杀疏螺旋体抗体的产生。当能够产生杀疏螺旋体抗体的淋巴结细胞与抗小鼠IFN-γ一起培养时,杀疏螺旋体抗体的产生增加了八倍。然而,对这些细胞进行抗IFN-γ处理也增强了它们适应性诱导关节炎的能力。当将经抗IFN-γ处理且产生杀疏螺旋体抗体的淋巴结细胞注入C3H/HeJ小鼠体内,然后用伯氏疏螺旋体攻击这些小鼠时,小鼠会发展出严重的破坏性莱姆关节炎。需要进行更多研究来阐明负责诱导关节炎和产生杀疏螺旋体抗体的免疫反应。需要这些研究来确保研发出一种有效且安全的抗伯氏疏螺旋体感染疫苗。