Passively transferred anti-MUC1 antibodies cause neither autoimmune disorders nor immunity against transplanted tumors in MUC1 transgenic mice
✍ Scribed by Richard M. Tempero; Gerald J. Rowse; Sandra J. Gendler; Michael A. Hollingsworth
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- French
- Weight
- 66 KB
- Volume
- 80
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
C57BL/6 mice transgenic for human MUC1 (MUC1.Tg) have been developed to investigate the autoimmune consequences of producing MUC1 tumor immunity in an animal that expresses MUC1 as a self-protein on normal ductal epithelia. Previous work showed that MUC1.Tg mice challenged with MUC1-bearing syngeneic tumors (B16.MUC1) developed progressively growing MUC1-expressing tumors and no detectable MUC1-specific antibody (Ab) response. In contrast, wild-type C57BL/6 (wt) mice developed MUC1negative tumors at a significantly slower rate and produced approximately 50 g IgG 1 Ab reactive with the MUC1 tandem repeat (TR)/ml of sera. One milliliter of these sera was administered passively to MUC1.Tg or wt mice and the concentration of the MUC1 TR-reactive IgG 1 Abs was monitored over time. The results indicate that circulating MUC1reactive Abs were detectable in MUC1.Tg mice and that significant amounts of these Abs were not absorbed by organs that endogenously express MUC1. No evidence of autoimmune disease, either gross or histological, was observed in the MUC1.Tg recipients of sera suggesting that MUC1, an organ-specific protein expressed primarily by secretory epithelia, is inaccessible to circulating MUC1-reactive Abs. Additional studies showed that polyclonal sera containing IgG 1 Abs reactive with MUC1 TR were unable to provide protection against the growth of syngeneic tumors expressing MUC1 in the MUC1.Tg animal model.