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National Public Health Institute and MediCity Research Laboratory, Turku University, 20520 Turku, Finland
CD73, otherwise known as ecto-5
-nucleotidase, is a glycosyl-phosphatidylinositol-linked 70-kD
molecule expressed on different cell types, including
vascular endothelial cells (EC) and certain subtypes of
lymphocytes. There is strong evidence for lymphocyte CD73 having a role in several immunological phenomena such as lymphocyte activation, proliferation, and
adhesion to endothelium, but the physiological role of
CD73 in other cell types is less clear. To compare the
biological characteristics of CD73 in different cell
types, we have studied the structure, function, and surface modulation of CD73 on lymphocytes and EC.
CD73 molecules on lymphocytes are shed from the cell
surface as a consequence of triggering with an antiCD73 mAb, mimicking ligand binding. In contrast, triggering of endothelial CD73 does not have any effect on
its expression. Lymphocyte CD73 is susceptible to
phosphatidylinositol phospholipase, whereas only a
small portion of CD73 on EC could be removed by this
enzyme. Furthermore, CD73 on EC was unable to deliver a tyrosine phosphorylation inducing signal upon
mAb triggering, whereas triggering of lymphocyte
CD73 can induce tyrosine phosphorylation. Despite the
functional differences, CD73 molecules on lymphocytes
and EC were practically identical structurally, when
studied at the protein, mRNA, and cDNA level. Thus,
CD73 is an interesting example of a molecule which
lacks structural variants but yet has a wide diversity of
biological functions. We suggest that the ligand- induced shedding of lymphocyte CD73 represents an
important and novel means of controlling lymphocyte-
EC interactions.
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