Hu B, Even C, Plagemann P G
Department of Microbiology, University of Minnesota Medical School, Minneapolis.
Viral Immunol. 1992 Spring;5(1):27-38. doi: 10.1089/vim.1992.5.27.
We have further investigated the nature of IgG-containing complexes of 150-300 kD that rapidly appear in the circulation of mice of various strains after infection with lactate dehydrogenase-elevating virus (LDV) and are recognized and quantitated by their binding in the presence of 0.05% Tween 20 to certain enzyme-linked immunosorbent assay (ELISA) plates with high protein affinity that have not been coated with protein antigen (5). These binding complexes have been found to contain primarily IgG2a or, in some mice, IgG2b. Their isotype specificity and time course of formation correlated with those of the polyclonal production of immunoglobulins in these mice, as measured by increases in total IgG2a or IgG2b in the circulation. In contrast, anti-LDV antibodies exhibited much broader isotype specificities in all mouse strains investigated. Depletion of BALB/c mice of CD4+T cells or lack of T cells in nude Swiss mice only partly reduced the polyclonal activation of B cells and the formation of ELISA plate-binding complexes, whereas anti-LDV antibody formation was completely blocked. Only a small proportion of the total IgG2a or IgG2b formed as a result of the LDV-induced polyclonal activation of B cells was recovered in plate-binding complexes, which sedimented in sucrose density gradients between 150 and 300 kD. Diverse monoclonal antibodies of different IgG isotopes did not bind to the plates at concentrations at which LDV-induced immune complexes exhibited binding activity. We suggest that the LDV-induced immune complexes do not contain anti-LDV antibodies, but are complexes of auto-antibodies and self-antigen(s). However, additional features must be responsible for the high affinity of these complexes for ELISA plates since various immune complexes formed in vitro failed to bind to the plates, and binding activity of the immune complexes formed in LDV-infected mice could not be regenerated in vitro once the complexes had been dissociated by a low pH treatment.
我们进一步研究了150 - 300 kD含IgG复合物的性质，这些复合物在感染乳酸脱氢酶升高病毒（LDV）后迅速出现在各种品系小鼠的循环系统中，并且在0.05%吐温20存在的情况下，通过它们与某些未包被蛋白质抗原、具有高蛋白亲和力的酶联免疫吸附测定（ELISA）板的结合来识别和定量（5）。已发现这些结合复合物主要含有IgG2a，在某些小鼠中含有IgG2b。它们的同种型特异性和形成的时间进程与这些小鼠中免疫球蛋白的多克隆产生相关，这通过循环中总IgG2a或IgG2b的增加来衡量。相比之下，在所有研究的小鼠品系中，抗LDV抗体表现出更广泛的同种型特异性。BALB/c小鼠的CD4⁺T细胞耗竭或裸瑞士小鼠缺乏T细胞仅部分降低了B细胞的多克隆激活和ELISA板结合复合物的形成，而抗LDV抗体的形成则被完全阻断。由于LDV诱导的B细胞多克隆激活而形成的总IgG2a或IgG2b中，只有一小部分在板结合复合物中回收，这些复合物在蔗糖密度梯度中沉降在150至300 kD之间。不同IgG同位素的多种单克隆抗体在LDV诱导的免疫复合物表现出结合活性的浓度下不与板结合。我们认为，LDV诱导的免疫复合物不包含抗LDV抗体，而是自身抗体和自身抗原的复合物。然而，这些复合物对ELISA板的高亲和力一定还有其他特征，因为体外形成的各种免疫复合物未能与板结合，并且一旦复合物通过低pH处理解离，LDV感染小鼠中形成的免疫复合物的结合活性在体外无法再生。
