Esaguy N, Freire O, Van Embden J D, Aguas A P
Center for Experimental Cytology, Abel Salazar Institute for the Biomedical Sciences, University of Porto, Portugal.
Scand J Immunol. 1993 Aug;38(2):147-52. doi: 10.1111/j.1365-3083.1993.tb01706.x.
We have recently reported antigenic (B-cell) cross-reactivity between the mycobacterial 65 kDa heat shock protein (hsp65) and human lactoferrin (LF) and we suggested that this cross-reactivity might have a role in mycobacteria-associated autoimmune disease. Here, we have searched for anti-LF T-cell reactivity in Lewis rats submitted to a mycobacteria-triggered autoaggressive disorder (adjuvant arthritis, AA), an autoimmune disorder characterized by high anti-hsp65 reactivity. We have quantified the in vitro proliferative response to LF of lymph node and spleen cells of Lewis rats killed 9, 14 and 21 days after the immunization with the AA-triggering, mycobacteria-containing adjuvant (complete Freund's adjuvant, CFA). We found that LF induced significant proliferation of lymph node T cells of rats undergoing AA. This T-cell proliferation was not as marked as the one provoked by hsp65; it was, nevertheless, significantly higher (P < 0.05) than that produced by a non-arthritogenic antigen (i.e. albumin). T cells from naive or mineral oil (incomplete Freund's adjuvant, IFA) injected rats did not respond to LF or hsp65. These data indicate that LF may work as an accessory stimulatory factor of the T-cell autoreactivity associated with mycobacteria-induced arthritis.
我们最近报道了分枝杆菌65 kDa热休克蛋白（hsp65）与人乳铁蛋白（LF）之间存在抗原性（B细胞）交叉反应，并且我们认为这种交叉反应可能在分枝杆菌相关的自身免疫性疾病中起作用。在此，我们在患有分枝杆菌引发的自身攻击性疾病（佐剂性关节炎，AA）的Lewis大鼠中寻找抗LF T细胞反应性，AA是一种以高抗hsp65反应性为特征的自身免疫性疾病。我们对在用引发AA的含分枝杆菌佐剂（完全弗氏佐剂，CFA）免疫后9、14和21天处死的Lewis大鼠的淋巴结和脾细胞对LF的体外增殖反应进行了定量。我们发现LF可诱导患AA大鼠的淋巴结T细胞显著增殖。这种T细胞增殖不如hsp65引发的增殖明显；然而，它显著高于（P<0.05）由非致关节炎抗原（即白蛋白）产生的增殖。来自未接触过抗原或注射了矿物油（不完全弗氏佐剂，IFA）的大鼠的T细胞对LF或hsp65无反应。这些数据表明，LF可能作为与分枝杆菌诱导的关节炎相关的T细胞自身反应性的辅助刺激因子。
