Shao Hui, Lei Song, Sun Sheher L, Xiang Jim, Kaplan Henry J, Sun Deming
Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center, University of Louisville, Louisville, KY 40202, USA.
J Immunol. 2003 Nov 1;171(9):4780-5. doi: 10.4049/jimmunol.171.9.4780.
Aberrant activation of autoreactive T cells is one of the major causes of autoimmune disease. Autoantigens are sequestered and in many cases weak immunogens. For example, in experimental autoimmune uveitis, immunization of naive rats with autologous interphotoreceptor retinoid-binding protein (IRBP) fails to induce intraocular inflammation or a strong T cell response, whereas bovine IRBP is a strong inducer of experimental autoimmune uveitis. Such observations challenge the view that the autoantigen alone is responsible for the development of autoimmunity. Here, we demonstrate that autologous rat IRBP is converted to a strong immunogen in the presence of a small dose of CpG-containing oligodeoxynucleotides. Our results indicate that specific CpG-containing oligodeoxynucleotides may play an important role in the activation and expansion of autoreactive T cells in vivo, leading to autoimmune disease.
自身反应性T细胞的异常激活是自身免疫性疾病的主要原因之一。自身抗原被隔离，在许多情况下是弱免疫原。例如，在实验性自身免疫性葡萄膜炎中，用自体视网膜色素上皮间维生素A结合蛋白（IRBP）免疫未致敏大鼠未能诱导眼内炎症或强烈的T细胞反应，而牛IRBP是实验性自身免疫性葡萄膜炎的强诱导剂。这些观察结果挑战了仅自身抗原就导致自身免疫性疾病发生的观点。在这里，我们证明在小剂量含CpG的寡脱氧核苷酸存在下，自体大鼠IRBP可转化为强免疫原。我们的结果表明，特定的含CpG寡脱氧核苷酸可能在体内自身反应性T细胞的激活和扩增中起重要作用，从而导致自身免疫性疾病。
