McKeever U, Khandekar S, Newcomb J, Naylor J, Gregory P, Brauer P, Jesson M, Bettencourt B, Burke E, Alderson A, Banerji J, Haskins K, Jones B
Procept Incorporated, Cambridge, Massachusetts 02139.
J Exp Med. 1996 Nov 1;184(5):1755-68. doi: 10.1084/jem.184.5.1755.
The BDC 2.5 T cell clone is specific for pancreatic beta-cell antigen presented by I-Ag7, and greatly accelerates diabetes when injected into 10-21-d-old nonobese diabetic (NOD) mice. The BDC 2.5 T cell receptor (TCR) has been solubilized as a TCR-IgG1 chimeric protein. All NOD mice immunized against BDC 2.5 TCR-IgG1 produced antibodies recognizing TCR C alpha/C beta epitopes that were inaccessible on the T cell surface. 56% of the mice produced antibodies against the BDC 2.5 clonotype that specifically blocked antigen activation of BDC 2.5 cells. We have used the adoptive transfer model of diabetes to demonstrate that maternal immunization with soluble TCR protects young mice from diabetes induced by the BDC 2.5 T cell clone.
BDC 2.5 T细胞克隆对由I-Ag7呈递的胰腺β细胞抗原有特异性，并且当注射到10至21日龄的非肥胖糖尿病（NOD）小鼠体内时会极大地加速糖尿病进程。BDC 2.5 T细胞受体（TCR）已被溶解为TCR-IgG1嵌合蛋白。所有针对BDC 2.5 TCR-IgG1免疫的NOD小鼠都产生了识别TCR Cα/Cβ表位的抗体，这些表位在T细胞表面是无法接近的。56%的小鼠产生了针对BDC 2.5克隆型的抗体，该抗体特异性地阻断了BDC 2.5细胞的抗原激活。我们利用糖尿病的过继转移模型证明，用可溶性TCR进行母体免疫可保护幼鼠免受BDC 2.5 T细胞克隆诱导的糖尿病。
