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首页> 外文期刊>Infection and immunity >Pathogen Specificity and Autoimmunity Are Distinct Features of Antigen-Driven Immune Responses in Neuroborreliosis
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Pathogen Specificity and Autoimmunity Are Distinct Features of Antigen-Driven Immune Responses in Neuroborreliosis

机译：病原体特异性和自身免疫性是神经源性硼中毒抗原驱动的免疫反应的不同特征。

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Neuroborreliosis (NB) is a chronic infectious disease of the central nervous system (CNS) caused by a tick-borne spirochete, Borrelia burgdorferi. In addition to direct effects of the causative infectious agent, additional immunity-mediated mechanisms are thought to play a role in the CNS pathology of NB. In order to further understand the involvement of humoral immune mechanisms in NB, we dissected the intrathecal antibody responses down to the single-plasma-cell level. Starting with single-cell reverse transcription-PCR of fluorescence-activated cell sorter-sorted cerebrospinal fluid plasma cells from an NB patient, we identified expanded clones and resurrected the antigen specificity of their secreted antibodies through recombinant expression of the correctly paired immunoglobulin heavy- and light-chain genes as monoclonal antibodies (MAbs). As expected, we found specificity for the causative infectious agent, B. burgdorferi, among the clonally expanded plasma cell (cePC)-derived MAbs. However, from an independent cePC of the same patient, we could derive MAbs specific for human CNS myelin, without detectable cross-reactivity with B. burgdorferi antigens. While reactivity against B. burgdorferi is a known feature of humoral immune responses in NB, we show (i) that immune responses specific for self antigens may be a distinct feature of CNS infections independent of pathogen reactivity and (ii) that humoral autoimmunity in NB (since found in cePC) is the result of a truly antigen-driven immune response. Our findings indicate that in NB mechanisms may be at play that induce distinct immune responses specific for pathogen and self antigens independent from “molecular mimicry.”
机译：神经硼化病（NB）是由壁虱传播的螺旋体 Borrelia burgdorferi 引起的中枢神经系统（CNS）慢性感染性疾病。除了引起病原体的直接作用外，其他免疫介导的机制也被认为在NB的CNS病理中起作用。为了进一步了解体液免疫机制在NB中的参与，我们解剖了鞘内抗体应答直至单浆细胞水平。从NB患者的荧光激活的细胞分选仪分选的脑脊髓液浆细胞的单细胞逆转录PCR开始，我们鉴定了扩展的克隆并通过正确表达配对的免疫球蛋白重链和重链的重组表达复活了其分泌抗体的抗原特异性。轻链基因作为单克隆抗体（MAb）。如预期的那样，我们发现了致病性传染病菌 B的特异性。克隆的浆细胞（cePC）衍生的单克隆抗体中的burgdorferi 。但是，从同一位患者的独立cePC中，我们可以衍生出对人CNS髓磷脂具有特异性的单克隆抗体，而没有与 B的交叉反应。 burgdorferi抗原。对 B具有反应性。 burgdorferi 是NB体液免疫反应的已知特征，我们证明（i）对自身抗原具有特异性的免疫反应可能是CNS感染的独立特征，与病原体反应无关，并且（ii）NB体液自身免疫（ （在cePC中发现）是真正的抗原驱动的免疫反应的结果。我们的研究结果表明，在NB机制中，可能会诱导与病原体和自身抗原不同的独特免疫应答，而独立于“分子拟态”。

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