The MHC class I-related FcRn ameliorates murine Lyme arthritis.
The MHC class I-related FcRn ameliorates murine Lyme arthritis.
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MHC I 类相关 FcRn 可改善小鼠莱姆关节炎。
DOI：
10.1093/intimm/dxh380
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Huber,BrigitteT
中科院分区：
文献类型：
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作者：
Crowley,Helena;Alroy,Joseph;Sproule,ThomasJ;Roopenian,Derry;Huber,BrigitteT
新生儿FcR（FcRn）作为IgG稳态调节剂的鉴定导致了旨在描绘FcRn在体液介导的疾病中的作用的研究。FcRn是I类相关分子，其通过在低pH下优先结合IgG并抑制其降解来延长血清IgG的半衰期。它在对感染性生物体的保护性免疫中的作用尚不清楚。我们研究了FcRn在由伯氏疏螺旋体感染引起的小鼠莱姆关节炎模型中的功能。我们用B. burgdorferiand监测关节炎的发展。感染FcRn−/−小鼠的血清抗B水平降低。伯氏螺旋体抗体和杀疏螺旋体活性。此外，这些突变小鼠在感染后出现踝关节肿胀和关节组织病理学增加。我们的数据表明，FcRn通过防止保护性杀疏螺旋体抗体的降解来改善小鼠莱姆病关节炎。
The identification of the neonatal FcR (FcRn) as an IgG homeostasis regulator has led to research aimed at delineating a role for FcRn in humorally mediated disease. FcRn is a class I-related molecule that prolongs the half-life of serum IgG by preferentially binding IgG at low pH and inhibiting its degradation. Its role in protective immunity to infectious organisms is unknown. We investigated the function of FcRn in the murine model of Lyme arthritis, caused by infection withBorrelia burgdorferi. We infected FcRn−/−and wild-type mice withB. burgdorferiand monitored the development of arthritis. Infected FcRn−/−mice demonstrated decreased serum levels of anti-B. burgdorferiantibodies and borreliacidal activity. Moreover, these mutant mice developed increased ankle swelling and joint histopathology following infection. Our data suggest that FcRn ameliorates murine Lyme arthritis by preventing the degradation of protective borreliacidal antibodies.