Zajkowska Joanna, Grygorczuk Sambor, Kondrusik Maciej, Pancewicz Sławomir, Hermanowska-Szpakowicz Teresa
Klinika Chorób Zakaźnych i Neuroinfekcji AM w Białymstoku.
Przegl Epidemiol. 2006;60 Suppl 1:167-70.
B. burgdorferi can evade the destructive effects of the immune system by binding host's complement regulators, which leads to inhibition of the complement activation cascade. Complement activity is blocked by CRASPs--complement regulator acquiring surface proteins. Complement resistance might therefore represent one major pathogenic factor favoring spirochete transmission to the vertebrate host, as well as determine host reservoirs of Borrelia burgdorferi genospecies. The cause of neuro-psychiatric disorders developing in some patients with Lyme borreliosis is still unknown. One of the hypotheses links them to neuro-hormonal disturbances induced by B. burgdorferi infection.
伯氏疏螺旋体可通过结合宿主补体调节因子来逃避免疫系统的破坏作用，这会导致补体激活级联反应受到抑制。补体活性被CRASPs（补体调节因子获取表面蛋白）所阻断。因此，补体抗性可能是有利于螺旋体传播至脊椎动物宿主的一个主要致病因素，同时也决定了伯氏疏螺旋体基因种的宿主储存库。部分莱姆病患者出现神经精神障碍的病因仍不明确。其中一种假说是将它们与伯氏疏螺旋体感染引起的神经激素紊乱联系起来。
