Saoudi A, Bellon B, de Kozak Y, Druet P
Pathologie rénale et vasculaire, INSERM U28, Hôpital Broussais, Paris, France.
Curr Eye Res. 1992;11 Suppl:101-5. doi: 10.3109/02713689208999518.
We previously demonstrated that mercuric chloride (HgCl2) injected-(Lewis x Brown-Norway) F1 rats are protected against experimental autoimmune uveoretinitis (EAU) induced by active immunization with the retinal S-antigen (S-Ag). To better understand the mechanisms of the protection promoted by HgCl2, we studied the effect of HgCl2-induced autoimmune disease on transferred EAU. We demonstrate herein that HgCl2 has no effect on adoptively transferred EAU. Therefore, the HgCl2-induced autoimmune disease does not affect effector S-Ag specific T cells activated in vitro but acts at an earlier stage.
我们之前证明,向(Lewis×Brown-Norway)F1大鼠注射氯化汞(HgCl2)可使其免受因用视网膜S抗原(S-Ag)主动免疫诱导的实验性自身免疫性葡萄膜视网膜炎(EAU)的侵害。为了更好地理解HgCl2所促进的保护机制,我们研究了HgCl2诱导的自身免疫性疾病对转移型EAU的影响。我们在此证明,HgCl2对过继转移的EAU没有影响。因此,HgCl2诱导的自身免疫性疾病并不影响体外激活的效应性S-Ag特异性T细胞,而是在更早阶段起作用。