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We report clear evidence that the interaction of the CD38 molecule with the specific mAb A10 on normal human cells and lines modulates the expression of surface activation markers relevant to T, NK, and plasma cell biology and functions. Moreover A10 mAb binding is followed by proliferation effects on all the target cells analyzed, and the phenomenon is accessory cell and IL-2 dependent. The effects of A10 mAb synergizing both CD2 and CD3 activation pathways indicate that CD38 signal transduction mechanism(s) are apparently different from the aforementioned. Nevertheless the decreased A10-driven proliferation after CD3-Ti modulation suggests a possible functional interdependence between these activation pathways. Taken together, the results indicate that the CD38 molecule might play a physiologic role in T, NK, and plasma cell regulation.


Journal article


J Immunol

Publication Date





2390 - 2396


ADP-ribosyl Cyclase, ADP-ribosyl Cyclase 1, Antibodies, Monoclonal, Antigens, CD, Antigens, Differentiation, Antigens, Differentiation, T-Lymphocyte, CD2 Antigens, CD3 Complex, Cell Division, Cell Line, Flow Cytometry, HLA-D Antigens, Humans, In Vitro Techniques, Killer Cells, Natural, Lymphocyte Activation, Membrane Glycoproteins, Plasma Cells, Receptors, Antigen, T-Cell, Receptors, Immunologic, Receptors, Interleukin-2, T-Lymphocytes, Tumor Cells, Cultured