Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was previously shown that CD26 (DPP IV, EC 3.4.14.5) is a binding site for adenosine deaminase (ADA, EC 3.5.4.4) on T cells and that costimulation by some anti-CD26 monoclonal antibodies (mAbs) and anti-CD3 induces CD4+ T cell proliferation. The CD26 epitopes involved in costimulation, the precise sequence of the events preceding proliferation, and the response of CD8+ compared with CD4+ T cells to CD26 were not extensively studied. We therefore compared the effects of the novel TA5.9 anti-CD26 mAb, recognizing an ADA-binding epitope, and the clearly distinct anti-Ta1 reference anti-CD26 mAb for their costimulatory properties in various T cell subsets. Both purified CD4+ and CD8+ T cells proliferated upon costimulation with anti-CD3 and either anti-CD26 mAb, but anti-TA5.9 mAb induced a more potent response than anti-Ta1. Either anti-CD26 mAb, together with anti-CD3, caused a similar sequential up-regulation of CD69, CD25 (IL-2R alpha), and CD71 (transferrin receptor) expression on CD4+ and CD8+ T cells. The activation markers appeared faster on the CD45R0+ than on the CD45R0- subsets. After costimulation, CD4+ T cell cultures contained significant amounts of the Th1 cytokines IL-2, interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha). In CD8+ T cell cultures relatively more IFN-gamma and TNF-alpha but almost no IL-2 was measured after triggering of CD3 and CD26. Our data demonstrate that the recognition of the ADA-binding epitope is not a prerequisite for the costimulatory capacity of anti-CD26 mAbs. Both CD4+ and CD8+ T cells and their CD45R0- and CD45R0+ subsets are sensitive to various aspects of activation via CD26, but the magnitude and/or kinetics differ according to the anti-CD26 used and the T cell subset studied.
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PMID:Costimulation of CD4+ and CD8+ T cells through CD26: the ADA-binding epitope is not essential for complete signaling. 766 88

Adenosine deaminase (ADA) expression on the surface of mitogen-stimulated lymphocytes was studied by flow cytometry. The gate for lymphocytes was located by cell size (forward scatter), cytoplasmic complexity (side scatter) and by expression of the markers CD2, CD4, CD8 and CD19. After mitogenic proliferation two populations appeared, one corresponding to non-stimulated cells, and the other consisting of larger cells which showed relatively high expression of adenosine deaminase on their surface. The increase was similar to that observed for CD71 expression, and paralleled the increase in 3H-thymidine incorporation. There was a correlation between ADA and CD71 expression (r = 0.92 for phytohaemagglutinin (PHA) and 0.97 for pokeweed mitogen (PWM)). These results suggest a role for ecto-adenosine deaminase in lymphocyte proliferation and/or triggering.
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PMID:Surface expression of adenosine deaminase in mitogen-stimulated lymphocytes. 834 57

Peripheral blood, bone marrow and/or lymph nodes of 77 patients with T- and B-ALLs/lymphomas were characterized for their surface membrane marker profiles using flow cytometry and fluorescence microscopy. Purine metabolism enzyme activities were compared with membrane immunophenotypes. T and B-ALLs/lymphomas subtypes were defined by the expression of surface membrane antigens detected by the monoclonal antibodies. Based on immunophenotyping we found the following characteristic marker profiles: in T-ALL-CD7, CD2, CD1, CD5, CD3, CD4, CD8, CD38, CD71; in T-NHL-CD7,CD2,CD3,CD4,CD5,CD6; in pre-B ALL-CD10, CD19, CD24, HLA-DR, CD34, in B-ALL-CD19, CD20, CD24, HLA-DR, SmIg with kappa or lamda light chains; in B-ALL-weak SmIg, kappa or lambda, CD19, CD20, CD24, CD5, HLA-DR; in B-NHL-CD19, CD20, CD22, CD24, CD5, more intensive SmIg, kappa or lambda. The cells of leukemic cases tended to have more immature phenotypes than those of lymphoma cases. Analysis of purine metabolism enzyme activities showed that there was a correlation between the values of adenosine deaminase (ADA) and purine nucleoside (PNP) and various types of T- and B-ALLs/lymphomas. ADA levels in B-NHL and B-CLL were lower than those in normal cells, while ADA level in T-ALL, T-NHL, pre-B-ALL and B-ALL was higher (the average 185,92,73,63 pkat. 10(-6)cells, respectively). ADA activity was significantly different between lymphocytes of control group and T-ALL(p<0.01), between T-ALL and T-NHL(p<0.05), between T-NHL and B-NHL(p<0.05) and between T-ALL and B-NHL(p<0.05). PNP activities were lower to those in normal cells. ADA/PNP ratio increased mostly in T-ALL, less in T-NHL, pre-B-ALL and B-ALL (10.8 and 5.3 and 2.2, and 2.0 respectively). ADA/PNP ratio was significantly different between T-ALL and pre-B-ALL(p<0.05) and between T-ALL and B-NHL(p<0.05).
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PMID:A comparison of some leucocyte differentiation markers and the adenosine deaminase and purine nucleoside phosphorylase values in B and T cell leukemias and lymphomas. 859 72