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Functional expression of CD43 on human natural killer cells
Author(s) -
Aguado Enrique,
Santamaría Manuel,
Gallego María Dolores,
Peña José,
Molina Ignacio J.
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.6.923
Subject(s) - cd43 , microbiology and biotechnology , biology , tyrosine phosphorylation , natural killer cell , lymphokine activated killer cell , interleukin 21 , phosphorylation , t cell , cytotoxic t cell , immunology , in vitro , biochemistry , immune system , antigen , cd20
CD43 is the major leukocyte sialoglycoprotein that plays important functional roles in neutrophils and lymphocytes. However, the expression of CD43 on human natural killer (NK) cells and its participation in the regulation of NK activity has not been studied. We have therefore investigated the expression of CD43 isoforms on human NK cell subpopulations as well as the role of this molecule in NK cell activation and cytotoxicity. We found that CD56 bright and CD56 dim NK cells express different sialylated forms of CD43, observing that activation of the CD56 bright NK cells induces the change of tetrasaccharide O ‐glycans to hexasaccha‐ride O ‐glycans on CD43. Cross‐linking of the molecule with mAbs results in a metalloprotease‐dependent loss of CD43 from the NK cell surface, whereas soluble anti‐CD43 mAbs induce a vigorous NK cell proliferation. This property is distinct from T cells, which proliferate after CD43 cross‐linking only in the presence of monocytes. Occupancy of the CD43 receptor on NK cells transduces specific signals, leading to enhanced killing activity and tyrosine phosphorylation and de‐phosphorylation of several substrates. We therefore propose that CD43 significantly contributes to the regulation of the NK cell function by participating in the control of effector/target interactions and, if pertinent, by transducing activation signals. J. Leukoc. Biol. 66: 923–929; 1999.