CD26 Surface Antigen Expression on Peripheral Blood T Lymphocytes from Children with Down's Syndrome (Trisomy 21)

Abstract

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.

CD3+/CD30+ Circulating T Lymphocytes Are Markedly Increased in Older Subjectswith Down’s Syndrome (Tr isomy 21)

“…ment in the DS thymus, i.e. lymphocyte depletion, diminution of the cortex, loss of corticomedullary demarcation and enlarged cystic Hassal's corpuscles within the thymic medulla [1]. As a consequence, an abnormal maturation in the thymic environment occurs resulting in phenotypical and functional abnormalities in blood T lymphocytes.…”

“…As a consequence, an abnormal maturation in the thymic environment occurs resulting in phenotypical and functional abnormalities in blood T lymphocytes. In fact, T cells from DS subjects show poor proliferation in response to phytomitogens, recall antigens and agonist MoAbs directed against the CD3 and CD2 surface structures [1]. An impairment in the early signalling events implicated in the engagement of T-cell membrane receptors by the stimulating ligands may be one of the mechanisms underlying the defective proliferative ability of trisomic T lymphocytes [5].…”

“…The reactivity of blood T cells (CD3+) to monoclonal antibodies (MoAbs) directed against the CD30 molecule was analyzed using a previously described [1] immunophenotyping which employed phycoerythrin-conjugated anti-CD30 (IgG1, Immunotech, Milan, Italy) and fluorescein-conjugated anti-CD3 (IgG2a, Ortho, Raritan, N.J., USA) MoAbs. In some experiments, fluorescein-conjugated anti-CD4 MoAb (IgG2a, Ortho) or anti-CD8 (IgG2a, Ortho) were used instead of anti-CD3 MoAb.…”

“…It is known that the blood of DS patients contains a spectrum of autoantibodies, as well as an altered ratio of immunoregulatory T-cell subsets [1], including an increased number of cells which display the Á‰ T-cell receptor heterodimer [2]. CD3+, a 105-to 120-kD transmembrane molecule previously termed Ki-1, is a cell surface cytokine receptor originally identified on Reed-Sternberg cells of Hodgkin's disease and a subset of T-cell lymphomas, commonly referred to as Ki-1+ lymphoma [3].…”

CD26/DPPIV and response to hepatitis B vaccination

“…It is clear that CD26/DPPIV is involved in multiple functional activities related with immune response. [10][11][12]14,15,22,[26][27][28][29][30][31][32][33][34][35][36][37].…”