Manheimer A, Bona C
Eur J Immunol. 1985 Jul;15(7):718-22. doi: 10.1002/eji.1830150715.
A profound inability to produce IgG anti-2,4,6-trinitrophenyl (TNP) antibodies during the secondary immune response elicited by a T-dependent antigen was observed in aged MLR/lpr mice. This unresponsiveness is associated with a significantly low indirect anti-TNP plaque-forming cell response and a weak in vitro anti-TNP response upon the culture of keyhole limpet hemocyanin-primed T cells and TNP-primed B cells in the presence of TNP. The markedly low IgG anti-TNP response observed in aged MLR/lpr mice cannot be related to the presence of rheumatoid factors which are observed during the secondary response, since MRL +/+ and 129/J mice, (non-autoimmune disease strains), also produce significant amounts of anti-gamma-globulin antibodies yet mount a strong IgG anti-TNP response.
在由T细胞依赖性抗原引发的二次免疫应答过程中，观察到老年MLR/lpr小鼠产生IgG抗2,4,6-三硝基苯（TNP）抗体的能力严重受损。这种无反应性与间接抗TNP空斑形成细胞反应显著降低以及在匙孔血蓝蛋白致敏的T细胞和TNP致敏的B细胞于TNP存在下培养时体外抗TNP反应较弱有关。在老年MLR/lpr小鼠中观察到的显著低水平的IgG抗TNP反应与二次反应期间观察到的类风湿因子的存在无关，因为MRL +/+和129/J小鼠（非自身免疫病品系）也产生大量抗γ-球蛋白抗体，但仍能产生强烈的IgG抗TNP反应。
