George Jacob, Adler Arnon, Barshack Iris, Keren Gad, Roth Arie
Department of Cardiology, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
Cardiovasc Pathol. 2004 Jul-Aug;13(4):221-4. doi: 10.1016/j.carpath.2004.02.002.
We evaluated the effect of pretreatment with complete Freund's adjuvant (CFA) on experimentally induced myocarditis concomitant with the assessment of antigen-specific properties of disease-triggering lymphocytes.
Rats pretreated with CFA a week prior to myosin immunization developed a significantly attenuated myocardial inflammation as compared to control-treated animals. Furthermore, prior administration of CFA virtually abolished histological evidence of myocarditis induced by transfer of antimyosin lymphocytes. CFA administered subcutaneously prior to myosin immunization resulted in a significant reduction in lymph node cell reactivity to myosin. Assessment of cultured medium from lymphocytes obtained from CFA-pretreated myosin-immunized rats revealed reduced levels of interferon gamma but an increased production of IL-10, suggesting an induction of a Thl to Th2 switch.
Thus, CFA treatment suppressed both myosin-induced as well as adoptively transferred myocarditis concomitant with induction of antigen-specific unresponsiveness to myosin and skewing of the immune response in favor of a Th2-dominated profile.
我们评估了用完全弗氏佐剂(CFA)预处理对实验性诱导的心肌炎的影响,并同时评估了引发疾病的淋巴细胞的抗原特异性特性。
与对照处理的动物相比,在肌球蛋白免疫前一周用CFA预处理的大鼠发生的心肌炎症明显减轻。此外,预先给予CFA实际上消除了由抗肌球蛋白淋巴细胞转移诱导的心肌炎的组织学证据。在肌球蛋白免疫前皮下给予CFA导致淋巴结细胞对肌球蛋白的反应性显著降低。对从经CFA预处理的肌球蛋白免疫大鼠获得的淋巴细胞的培养基评估显示,干扰素γ水平降低,但白细胞介素-10的产生增加,提示诱导了从Th1向Th2的转变。
因此,CFA治疗抑制了肌球蛋白诱导的以及过继转移的心肌炎,同时诱导了对抗肌球蛋白的抗原特异性无反应性,并使免疫反应偏向以Th2为主的模式。