Antigen presentation abrogated in cells expressing truncated Ia molecules.

作者：N Nabavi, Zoher Ghogawala, ASHLEY B MYER, I J Griffith, William F. Wade, Z Z Chen, DAVID J. McKEAN, L H Glimcher · 发表于：The Journal of Immunology · 年份：1989 · DOI：10.4049/jimmunol.142.5.1444 · 被引用次数：79 · 研究领域：Monoclonal and Polyclonal Antibodies Research、T-cell and B-cell Immunology、Cell Adhesion Molecules Research

Oligonucleotide site-directed mutagenesis was used to introduce a premature stop codon in wildtype A beta k and A alpha k cDNA clones to create truncated A beta k and A alpha k molecules lacking the cytoplasmic domain. Transfected B lymphoma cells expressing an I-Ak molecule with a truncated beta-chain or with truncated alpha- and beta-chains showed profound defects in two Ia-related functions: Ia-restricted Ag presentation and intracytoplasmic signaling. The ability of these transfected cell lines to activate autoreactive T hybrids was markedly impaired whereas loss of Ag presentation to nominal Ag-specific T hybrids was more subtle. Ia-mediated transmembrane signaling as measured by PKC translocation from cytosol to nucleus after stimulation with anti-Ak antibody was greatly affected by truncation of the A beta and A alpha cytoplasmic domains. These results indicate an important role for the highly conserved cytoplasmic domain in Ia-mediated responses.