Lim L C, England D M, Glowacki N J, DuChateau B K, Schell R F
Wisconsin State Laboratory of Hygiene, University of Wisconsin, Madison 53706, USA.
Infect Immun. 1995 Dec;63(12):4818-25. doi: 10.1128/iai.63.12.4818-4825.1995.
We determined that Borrelia burgdorferi-specific CD4+ T lymphocytes are responsible for the development of severe destructive Lyme arthritis and affect the production of borreliacidal antibody. Severe destructive Lyme arthritis was readily evoked in immunocompetent inbred LSH hamsters vaccinated with a whole-cell preparation of Formalin-inactivated B. burgdorferi sensu stricto isolate C-1-11 in adjuvant when challenged with B. burgdorferi sensu stricto isolate 297. When vaccinated hamsters were depleted of CD4+ T lymphocytes by the administration of monoclonal antibody GK1.5 and challenged, they failed to develop severe destructive arthritis. Similarly, nonvaccinated hamsters with or without the depletion of CD4+ T lymphocytes failed to develop severe destructive arthritis. In addition, depleting CD4+ T lymphocytes impaired the development of borreliacidal antibody in vaccinated and nonvaccinated hamsters challenged with the Lyme borreliosis spirochete. These findings show that CD4+ T lymphocytes are important for the recognition of arthritogenic and protective antigens of B. burgdorferi sensu lato isolates. Additional studies are needed to define the mechanisms responsible for the development of severe destructive Lyme arthritis and the production of borreliacidal antibody.
我们确定,伯氏疏螺旋体特异性CD4+ T淋巴细胞是导致严重破坏性莱姆关节炎发展的原因,并影响杀伯氏疏螺旋体抗体的产生。在用福尔马林灭活的严格意义上的伯氏疏螺旋体菌株C-1-11全细胞制剂加佐剂免疫的具有免疫能力的近交LSH仓鼠中,当用严格意义上的伯氏疏螺旋体菌株297攻击时,很容易诱发严重破坏性莱姆关节炎。当给接种疫苗的仓鼠注射单克隆抗体GK1.5以耗尽CD4+ T淋巴细胞后再进行攻击时,它们未能发展出严重破坏性关节炎。同样,无论是否耗尽CD4+ T淋巴细胞,未接种疫苗的仓鼠都未能发展出严重破坏性关节炎。此外,耗尽CD4+ T淋巴细胞会损害接种疫苗和未接种疫苗且受到莱姆病螺旋体攻击的仓鼠中杀伯氏疏螺旋体抗体的产生。这些发现表明,CD4+ T淋巴细胞对于识别广义伯氏疏螺旋体菌株的致关节炎和保护性抗原很重要。需要进一步研究来确定导致严重破坏性莱姆关节炎发展和杀伯氏疏螺旋体抗体产生的机制。