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首页> 外文期刊>Infection and immunity >Interleukin-4 (IL-4) and IL-13 Signaling Pathways Do Not RegulateBorrelia burgdorferi-Induced Arthritis in Mice: IgG1 Is Not Required for Host Control of Tissue Spirochetes
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Interleukin-4 (IL-4) and IL-13 Signaling Pathways Do Not RegulateBorrelia burgdorferi-Induced Arthritis in Mice: IgG1 Is Not Required for Host Control of Tissue Spirochetes

机译：白细胞介素4（IL-4）和IL-13信号传导途径不能调节小鼠博氏疏螺旋体诱发的关节炎：组织螺旋体的宿主控制不需要IgG1

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Previous studies have suggested that interleukin-4 (IL-4) has a protective effect in host defense to Borrelia burgdorferiinfection, both in limiting the severity of arthritis and in controlling spirochete numbers in tissues, and a mapping study revealed suggestive linkage to a cluster of genes on mouse chromosome 11, including the genes for IL-4 and IL-13. In contrast, other studies have questioned the importance of IL-4. In this study the involvement of IL-4 in murine Lyme disease was examined in C57BL/6J and BALB/cJ mice with targeted disruptions in the IL-4 gene, the IL-4Rα chain gene, or both. A spectrum of arthritis severity was seen in BALB/cJ mice, and ablation of IL-4, IL-4Rα, or both had no effect on the overall severity of arthritis as determined by joint swelling and histopathology. Wild-type C57BL/6J mice exhibited mild to moderate arthritis, and ablation of IL-4 again had no effect on arthritis severity. IL-4- and IL-4Rα-deficient mice produced extremely low levels of immunoglobulin G1 (IgG1) and showed increased production of IgG2b. This shift in immunoglobulin isotype had no effect on the host's ability to control spirochete growth in either strain of mouse, as determined by PCR detection of B. burgdorferi DNA from heart and ankle tissues. In summary, the IL-4-IL-4Rα pathway, including IL-13 signaling, neither limits arthritis severity nor is required for control of spirochete growth during B. burgdorferi infection of mice. Furthermore, the IgG1 isotype is not required to control B. burgdorferi cell numbers in tissues. These findings suggest the host defense against B. burgdorferi infection is not dependent on the Th1-Th2 paradigm of T-cell responses.
机译：先前的研究表明，白介素4（IL-4）在宿主防御伯氏疏螺旋体中具有保护作用，既可以限制关节炎的严重程度，又可以控制组织中的螺旋体数目，研究表明暗示性链接到小鼠11号染色体上的一组基因，包括IL-4和IL-13的基因。相反，其他研究质疑IL-4的重要性。在这项研究中，在C57BL / 6J和BALB / cJ小鼠中检测了IL-4参与鼠类莱姆病的情况，其中IL-4基因和/或IL-4Rα链基因或两者均被靶向破坏。在BALB / cJ小鼠中观察到了一系列的关节炎严重程度，通过关节肿胀和组织病理学测定，消融IL-4，IL-4Rα或两者对关节炎的总体严重程度没有影响。野生型C57BL / 6J小鼠表现出轻度至中度的关节炎，而IL-4的消融对关节炎的严重程度也没有影响。 IL-4-和IL-4Rα缺陷型小鼠产生极低水平的免疫球蛋白G1（IgG1），并显示IgG2b产生增加。免疫球蛋白同种型的这种变化对宿主控制任一小鼠品系中螺旋体生长的能力没有影响，这是通过PCR检测B来确定的。心脏和脚踝组织中的burgdorferi DNA。总之，IL-4-IL-4Rα途径，包括IL-13信号传导，既没有限制关节炎的严重性，也没有控制 B期间螺旋体生长的要求。博格多夫氏菌感染小鼠。此外，不需要IgG1同种型来控制 B。 burgburgeri 组织中的细胞数。这些发现表明宿主抗 B。 burgdorferi 感染不依赖于T细胞反应的Th1-Th2范式。

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