Carbohydrate recognition on MUC1-expressing targets enhances cytotoxicity of a T cell subpopulation.

Journal Article (Journal Article)

The influence of the epithelial mucin MUC1 on T cell-mediated lysis was analysed using lymph node lymphocytes (LNL) from patients with colorectal carcinoma. LNL were stimulated with allogeneic, MUC1-transfected B cells and the bulk cultures were cloned. Alloreactive cytotoxic T cell clones were obtained which preferentially lysed MUC1-expressing targets. The majority was CD4+ and MHC-class II-restricted, and a minor group was CD8+ and MHC-class I-restricted. All the clones expressed CD3 and TCR alpha beta, and were CD56-. The capacity to preferentially kill MUC1-expressing targets was stable in several clones for up to 6 months in culture. The enhancing effect of MUC1 on the lysis was investigated in more detail. It was only seen after inhibition of O-linked glycosylation in the targets. Furthermore, this effect was completely abrogated by the monoclonal antibody 3C9, directed against the Thomsen-Friedenreich antigen (T-antigen, Gal beta 1-3GalNAc bound alpha 1-3 to Ser/Thr) as well as by the soluble disaccharide Gal beta 1-3GalNAc, but not by other similar disaccharides. The authors conclude that in their system the preferential killing of MUC1-expressing targets is due to the recognition of an internal carbohydrate epitope accessible on under-glycosylated MUC1, possibly T-antigen, by an auxiliary receptor molecule on T cells.

Full Text

Duke Authors

Cited Authors

  • Böhm, CM; Mulder, MC; Zennadi, R; Notter, M; Schmitt-Gräff, A; Finn, OJ; Taylor-Papadimitriou, J; Stein, H; Clausen, H; Riecken, EO; Hanski, C

Published Date

  • July 1997

Published In

Volume / Issue

  • 46 / 1

Start / End Page

  • 27 - 34

PubMed ID

  • 9246205

International Standard Serial Number (ISSN)

  • 0300-9475

Digital Object Identifier (DOI)

  • 10.1046/j.1365-3083.1996.d01-91.x


  • eng

Conference Location

  • England