Pettinelli C B, Fritz R B, Chou C H, McFarlin D E
J Immunol. 1982 Sep;129(3):1209-11.
GPBP was shown to be encephalitogenic in SJL mice by direct challenge and in experiments in which an adoptive transfer system was employed. The three fragments obtained by treating GPBP with pepsin were assessed in the same manner. The encephalitogenic activity resided in the C terminal half of the molecule (residues 89-169). LNC also proliferated to the same fragment in vitro. Fragments 1-37, and, to a lesser extent, 44-48 stimulated sensitized LNC to proliferate but did not induce disease.
通过直接攻击以及采用过继转移系统的实验表明,GPBP在SJL小鼠中具有致脑炎作用。用胃蛋白酶处理GPBP得到的三个片段也以同样的方式进行了评估。致脑炎活性存在于分子的C端一半(第89 - 169位氨基酸残基)。LNC在体外对相同的片段也有增殖反应。第1 - 37位氨基酸残基片段,以及程度较轻的第44 - 48位氨基酸残基片段能刺激致敏的LNC增殖,但不会诱发疾病。