CD26 SURFACE-ANTIGEN EXPRESSION ON PERIPHERAL-BLOOD T-LYMPHOCYTES FROM CHILDREN WITH DOWNS-SYNDROME (TRISOMY-21)

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 nontranslocated 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.