Borel Y, Greene M I
Ann N Y Acad Sci. 1982;392:167-77. doi: 10.1111/j.1749-6632.1982.tb36106.x.
Here we describe a new model to elicit cellular immunity and induce unresponsiveness to nucleic acid antigens. Delayed-type hypersensitivity could be elicited by immunizing and challenging Balb/c mice with either guanosine-coupled spleen cells (G-SC) or adenosine-coupled spleen cells (A-SC) measured by footpad swellings. The epitope density was critical for immunization. This cellular reaction was specific to nucleosides, and crossimmunity was observed beween A-SC and G-SC. In addition, crossunresponsiveness was observed between these two nucleosides. In contrast, soluble carrier proteins coupled with either guanosine or adenosine did not induce crossreactive immunity or unresponsiveness. This emphasizes the dichotomy in both the mechanism and the specificity of unresponsiveness induced by the same ligand bound to two different self molecules (such as cell or igG). Finally, cellular immunity to nucleic acid antigens might be useful in ascertaining its involvement in experimental systemic lupus.
在此,我们描述了一种引发细胞免疫并诱导对核酸抗原无反应性的新模型。通过用鸟苷偶联的脾细胞(G-SC)或腺苷偶联的脾细胞(A-SC)免疫并攻击Balb/c小鼠,通过足垫肿胀测量可引发迟发型超敏反应。表位密度对免疫至关重要。这种细胞反应对核苷具有特异性,并且在A-SC和G-SC之间观察到交叉免疫。此外,在这两种核苷之间观察到交叉无反应性。相比之下,与鸟苷或腺苷偶联的可溶性载体蛋白不会诱导交叉反应性免疫或无反应性。这强调了与结合到两种不同自身分子(如细胞或IgG)上的相同配体诱导的无反应性在机制和特异性上的二分法。最后,对核酸抗原的细胞免疫可能有助于确定其在实验性系统性红斑狼疮中的作用。