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The Role of Viral Glycoproteins in Mumps Virus‐Mediated Antibody‐Dependent Cellular Cytotoxity in Vitro
Author(s) -
ALSHEIKHLY A.R.,
ORVELL C.,
WØHLIN B.,
ANDERSSON T.,
PERLMANN P.
Publication year - 1984
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1984.tb01024.x
Subject(s) - antibody dependent cell mediated cytotoxicity , antibody , monoclonal antibody , virology , glycoprotein , virus , mumps virus , microbiology and biotechnology , lysis , biology , in vitro , effector , cytotoxicity , chemistry , immunology , biochemistry
Treatment of human peripheral blood lymphocytes with live or UV‐inactivated mumps virions enhances antibody‐mediated cellular cytotoxicity (ADCC), reflected by increased target cell lysis in a 51 Cr‐release assay or an increased number of plaque‐forming cells on monolayers of bovine erythrocytes (E b ) in the presence of anti‐E b antibodies. Virus treatment of the E b targets causes a similar enhancement. The role of viral glycoproteins in ADCC enhancement was investigated by using a panel of monoclonal antibodies raised in mice against mumps virions. Most of the lymphocytes bound mumps virions, as ascertained by indirect immunofluorescence. A high proportion of virus‐treated lymphocytes also formed rosettes with E b . Anti‐HN antibodies inhibited resetting to various degrees. Although antibodies with high haemagglutination inhibition titres were most efficient inhibitors, antibodies without this serological activity were also inhibitory. Anti‐F antibodies were only weakly inhibitory, and anti‐NP antibodies had no effect. Anti‐HN antibodies also abrogated target cell lysis in the 51 Cr‐release assay and effector cell recruitment in the ADCC plaque assay by inhibiting virus‐mediated E b ‐lymphocyte interactions both at the target cell and at the effector cell level. Anti‐F or anti‐NP antibodies were only weakly or not at all inhibitory. The results suggest that virus‐mediated enhancement of ADCC is caused by the HN glycoprotein, primarily (although perhaps not exclusively) by its improvement of the effector cell‐target cell contacts necessary for the efficient execution of target cell lysis.