Paque R E, Miller R
Department of Microbiology, University of Texas Health Science Center, San Antonio 78284-7758.
Infect Immun. 1992 Aug;60(8):3396-404. doi: 10.1128/iai.60.8.3396-3404.1992.
Syngeneic mice receiving adoptively transferred enriched B cells or splenocytes pulsed in vitro with polyclonal anti-idiotypic antibodies (anti-Ids) against anti-CVB3 virus antibodies developed coxsackievirus B3 antigen-binding and virus-neutralizing antibodies during a 30-day period, in addition to overt expression of autoimmune myocarditis. Adoptive transfer of anti-Id pulsed T cells resulted in delayed appearance and transient expression of antiviral antibodies, and antiviral antibodies were marginal to absent in syngeneic animals receiving anti-Id pulsed macrophage populations. Proliferation analysis of recipient splenocytes indicated lack of proliferative capacity in response to monoclonal or polyclonal anti-Ids and only marginal proliferative capacity in response to coxsackievirus B3 virus antigen(s). In vitro assessment of delayed hypersensitivity in recipient animals demonstrated some specific immunity to anti-Ids in recipients receiving splenocytes or T cells. Anti-Ids expressing mimicry for heart-associated and/or viral antigen(s) interacting with B cells or other accessory cells suggest an autoantibody or anti-Id triggering of B-cell-mediated mechanisms involved in the development of myocarditis.
接受过体外用针对抗柯萨奇病毒B3（CVB3）病毒抗体的多克隆抗独特型抗体（抗-Id）脉冲处理的富集B细胞或脾细胞过继转移的同基因小鼠，在30天内产生了柯萨奇病毒B3抗原结合抗体和病毒中和抗体，此外还出现了明显的自身免疫性心肌炎。抗-Id脉冲处理的T细胞过继转移导致抗病毒抗体出现延迟且表达短暂，而在接受抗-Id脉冲处理的巨噬细胞群体的同基因动物中，抗病毒抗体极少或不存在。受体脾细胞的增殖分析表明，其对单克隆或多克隆抗-Id无增殖能力，对柯萨奇病毒B3病毒抗原的增殖能力也很微弱。对受体动物迟发型超敏反应的体外评估显示，接受脾细胞或T细胞的受体对抗-Id有一定的特异性免疫。表达与心脏相关和/或病毒抗原相似性的抗-Id与B细胞或其他辅助细胞相互作用，提示自身抗体或抗-Id触发了参与心肌炎发生发展的B细胞介导机制。
