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Unglycosylated Mtaa expresses an Mtab-like determinant.
Immunogenetics
|January 1, 1987
Summary
Maternally transmitted antigen (Mta) polymorphism is linked to mitochondrial factors. This study suggests N-linked glycosylation prevents Mta expression, revealing a novel mechanism for Mta antigenic variation.
Area of Science:
- Immunology
- Mitochondrial Genetics
- Molecular Biology
Background:
- Antigenic polymorphism in maternally transmitted antigen (Mta) is regulated by a maternally transmitted factor (Mtf), likely located in mitochondria.
- The precise mechanisms by which Mtf generates Mta antigenic polymorphism remain unclear.
Purpose of the Study:
- To investigate the role of posttranslational oligosaccharide addition in the formation of Mta determinants.
- To explore how Mtf contributes to Mta polymorphism through glycosylation.
Main Methods:
- Examined Mta expression on cytotoxic T lymphocyte (CTL) target cells cultured with tunicamycin (TM), an inhibitor of N-linked glycosylation.
- Tested lysis of TM-treated Mtaa targets by Mtab-specific CTL lines.
- Utilized a specific CTL clone (17D5.G2) to assess Mtab-like determinant expression on various Mtaa strains and Mta null cells.
Main Results:
- Eight of 18 Mtab-specific CTL lines lysed TM-treated Mtaa targets.
- A subclone (17D5.G2) lysed TM-treated targets from all tested Mtaa strains, irrespective of H-2K/D haplotype.
- This CTL clone did not lyse TM-treated target cells from Mta null strains, indicating Mtab-like determinant expression is concordant with Mtaa expression.
Conclusions:
- Data suggest an Mtab-like determinant is expressed on unglycosylated Mtaa molecules.
- N-linked oligosaccharides likely inhibit the expression of Mtab-like determinants on Mtaa.
- Mtf may influence Mta polymorphism via glycosylation pathways.