Weremeichik H, Moraska A, Herzum M, Weller A, Huber S A
Department of Pathology, University of Marburg, Federal Republic of Germany.
Eur Heart J. 1991 Aug;12 Suppl D:154-7. doi: 10.1093/eurheartj/12.suppl_d.154.
Coxsackievirus B3 (CVB3) infections induce myocardial inflammation which is presumably mediated by autoimmune mechanisms in the experimental murine model. Naturally occurring antibodies that also bind to myocytes have been identified that can either abrogate or enhance cardiac injury by modulating the immune response. Monoclonal antibodies derived from CVB3-infected mice were immobilized to plastic and overlaid with spleen cells obtained from mice infected with 5 x 10(4) plaque forming units of CVB3 0 to 8 days earlier. Controls consisted of either myocytes or virus adsorption monolayers. After incubation, non-adherent lymphocytes were removed, the adherent cells were recovered and cultured on either virus or myocytes for 48 h at 37 degrees C. The lymphocytes were removed and any antibody binding to the virus or myocytes was detected using goat anti-mouse IgG and IgM in a urease enzyme-linked immunoadsorption assay (ELISA). The original unfractionated spleen cell population added directly to the ELISA wells showed reactivity to both virus and myocytes. Cells adsorbed to myocytes made primarily myocyte-reactive antibody and cells adsorbed to virus made primarily virus-reactive antibody. Cells adsorbed to the heart-reactive mAB (10A1) made primarily virus-specific antibody suggesting this autoantibody might be an anti-idiotype of the virus-reactive response.
柯萨奇病毒B3（CVB3）感染可诱发心肌炎症，在实验性小鼠模型中，这种炎症可能是由自身免疫机制介导的。已经鉴定出也与心肌细胞结合的天然存在的抗体，这些抗体可通过调节免疫反应来减轻或加重心脏损伤。将源自CVB3感染小鼠的单克隆抗体固定在塑料上，并用0至8天前感染了5×10⁴蚀斑形成单位CVB3的小鼠的脾细胞覆盖。对照包括心肌细胞或病毒吸附单层。孵育后，去除未粘附的淋巴细胞，回收粘附细胞，并在病毒或心肌细胞上于37℃培养48小时。去除淋巴细胞，并在脲酶酶联免疫吸附测定（ELISA）中使用山羊抗小鼠IgG和IgM检测与病毒或心肌细胞结合的任何抗体。直接添加到ELISA孔中的原始未分级脾细胞群体对病毒和心肌细胞均有反应性。吸附到心肌细胞上的细胞主要产生与心肌细胞反应的抗体，而吸附到病毒上的细胞主要产生与病毒反应的抗体。吸附到心脏反应性单克隆抗体（10A1）上的细胞主要产生病毒特异性抗体，表明这种自身抗体可能是病毒反应性应答的抗独特型抗体。
