Revelli S S, Bottasso O A, Moreno H S, Davila H O, Amerio N, Morini J C
División Immunología, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Argentina.
Braz J Med Biol Res. 1990;23(6-7):567-71.
In the present study we investigated whether the attenuating effect of chronic Trypanosoma cruzi (Tc) infection on adjuvant arthritis (AA) in the rat could be transferred to naive recipients. Transfer of whole spleen cells, but not of serum, from Tc-infected rats reduced AA (means +/- SEM: 11 +/- 0.5) in recipient animals (control values, means +/- SEM: 19 +/- 0.7). Transfer of a T-cell-enriched subpopulation from spleen cells of Tc-infected rats (obtained by filtration through a nylon wool column) resulted in a similar attenuation of AA (means +/- SEM: 7.5 +/- 2.2). The arthritic response of rats intraperitoneally inoculated with 2 x 10(5) Tc 48 h before induction did not differ from that observed in controls. Neither parasites nor specific antibodies were observed in suckling mice inoculated with serum or cell suspensions employed in transfer experiments. Consequently, the depressive effect on AA could not be directly attributed to Tc per se. We hypothesize that a homeostatic immunosuppressor mechanism may be responsible for this phenomenon.
在本研究中,我们调查了慢性克氏锥虫(Tc)感染对大鼠佐剂性关节炎(AA)的减轻作用是否能转移给未感染的受体。将感染Tc大鼠的全脾细胞而非血清进行转移,可减轻受体动物的AA(平均值±标准误:11±0.5)(对照值,平均值±标准误:19±0.7)。将感染Tc大鼠脾细胞中富含T细胞的亚群(通过尼龙毛柱过滤获得)进行转移,也导致了类似程度的AA减轻(平均值±标准误:7.5±2.2)。在诱导前48小时腹腔接种2×10⁵个Tc的大鼠的关节炎反应与对照组观察到的反应无差异。在用转移实验中使用的血清或细胞悬液接种的乳鼠中未观察到寄生虫或特异性抗体。因此,对AA的抑制作用不能直接归因于Tc本身。我们推测一种稳态免疫抑制机制可能是造成这种现象的原因。