CD26 surface antigen expression on peripheral blood T lymphocytes from children with Down's syndrome (trisomy 21)
| Autor: | R. Britta, G. Castellucci, R Gerli, R. Vaccaro, C Vagliasindi, G. Giorgi, G. Fabietti, S. Crupi, Alberto Bertotto, C Muscat, N Forenza, F. M. Benedictis, Fabrizio Spinozzi |
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| Rok vydání: | 1994 |
| Předmět: |
Antigens
Differentiation T-Lymphocyte Male Adolescent CD3 Complex medicine.drug_class CD3 Dipeptidyl Peptidase 4 T-Lymphocytes Immunology CD2 Antigens Protein tyrosine phosphatase Monoclonal antibody Dipeptidyl peptidase Immunophenotyping Antigen medicine Humans Receptors Immunologic Child biology Antibodies Monoclonal Infant General Medicine T lymphocyte medicine.disease Flow Cytometry Molecular biology Polyclonal antibodies Child Preschool biology.protein Female Down Syndrome Trisomy |
| Zdroj: | Scandinavian journal of immunology. 39(6) |
| ISSN: | 0300-9475 |
| Popis: | A phenotypical analysis carried out by two-colour flow cytometry showed that the proportion of circulating CD4+ T lymphocytes co-expressing the membrane-associated ectoenzyme dipeptidyl peptidase IV (CD26 antigen), a functional collagen receptor involved in T-cell triggering through its interaction with the CD45 protein tyrosine phosphatase, was significantly lower in 28 children with non-translocated trisomy 21 (Down's syndrome) (DS) than that calculated in the bloodstream of 27 age- and sex-matched healthy controls. Agonist anti-CD26 monoclonal antibodies (MoAbs), such as anti-1F7, not only modulate the surface expression of this molecule, but also enhance the proliferative activity of normal human T cells via the CD3- and CD2-mediated activation pathways. T-lymphocyte proliferation induced by antigen or polyclonal T-cell activators, including anti-CD3 or -CD2 MoAbs, is severely impaired in DS. Although the physiological ligand of CD26 surface structure is unknown, the fact that CD4+ T lymphocytes found in the blood of trisomic subjects are mostly CD26- (anti-1F7-) suggests that their faulty mitogenic response may be due to phenotypical and, perhaps, strictly correlated functional abnormalities. |
| Databáze: | OpenAIRE |
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