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Expression of Dipeptidylpeptidase IV (DPP IV/CD26) Activity on Human Myeloid and B Lineage Cells, and Cell Growth Suppression by the Inhibition of DPP IV Activity

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Cellular Peptidases in Immune Functions and Diseases

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 421))

Abstract

Human CD26 antigen is a transmembrane glycoprotein with dipeptidyl peptidase IV (DPP IV) activity in its extracellular domain. Within the hematopoietic system, CD26/DPP IV has been thought to be exclusively expressed in activated T and NK cells [1]. However, by enzymatic assay, Bauvois et al. have characterized DPP IV activity (sensitive to diprotin A which is the specific inhibitor of DPP IV) present on the surface of human myeloblastic HL-60 and monoblastic U937 cell lines as well as on peripheral monocytes, granulocytes and macrophages [2]. Moreover, DPP IV activity increased strictly on cells undergoing macrophage maturation [2]. Reinhold et al. found that synthetic reversible inhibitors of DPP IV suppressed cell proliferation and modulated cytokine production in U937 cells expressing high levels of CD26 [3]. Monoclonal antibody (mAb) anti-Tal (purchased from Coulter, Hialeah, FL) and directed against CD26 of activated human T cells was recently shown to react with a few B cell lines including Daudi cells which are tumor cells derived from Burkitt lymphoma and EBV-transformed cells [4]. Another anti-CD26 mAb i.e. anti-TA5.9 (from Eurogenetics, Tessenderlo, Belgium) was shown to bind activated T cells as well as myeloid cells, Raji and U266 cells [5].

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References

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© 1997 Springer Science+Business Media New York

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Micouin, A., Bauvois, B. (1997). Expression of Dipeptidylpeptidase IV (DPP IV/CD26) Activity on Human Myeloid and B Lineage Cells, and Cell Growth Suppression by the Inhibition of DPP IV Activity. In: Ansorge, S., Langner, J. (eds) Cellular Peptidases in Immune Functions and Diseases. Advances in Experimental Medicine and Biology, vol 421. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9613-1_26

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  • DOI: https://doi.org/10.1007/978-1-4757-9613-1_26

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4757-9615-5

  • Online ISBN: 978-1-4757-9613-1

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