Monocytes rather than NK-cells contribute to antibody mediated protection from MCMV infection

Abstract

Event Abstract Back to Event Monocytes rather than NK-cells contribute to antibody mediated protection from MCMV infection Anna Bootz1*, Thomas Winkler2 and Michael Mach1 1 Institute for Clinical and Molecular Virology, Friedrich-Alexander university Erlangen-Nürnberg,, Germany 2 Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander university Erlangen-Nürnberg, Germany Cytomegalovirus is a clinically important pathogen. Previously we could show using murine cytomegalovirus (MCMV) that the adoptive transfer of immune serum into B- and T-cell deficient Rag-/- mice was highly effective against MCMV-induced morbidity and mortality. Antibodies can act either by direct neutralization of extracellular virus and/or by Fcγ receptor (FcγR)-mediated effector functions e.g. antibody-dependent cellular cytotoxicity (ADCC) and/or complement-dependent cytotoxicity (CDC). To analyze the contribution of the FcγRs we used animals lacking the FcRγ-chain (FcγRxRag-/-), which is the accessory chain of the activating murine IgG receptors FcγRI, FcγRIII and FcγRIV. Following serum therapy, FcγRxRag-/- mice developed high viral titers and showed a significantly shorter survival compared to the Rag-/- control mice indicating a substantial contribution of the Fcγ receptors in antibody protection. Animals lacking FcγRI, FcγRIII or FcγRIV individually were completely protected after immune serum therapy. Thus, NK cells which express only the FcγRIII seem not to participate significantly in antibody-mediated protection from MCMV. The depletion of NK cells in recipient mice confirmed this assumption. Mice lacking both, the FcγRIV and FcγRIII receptor developed high viral titers following serotherapy indicating redundant functions of the various FcγRs. Interestingly, adoptively transferred CD115+ monocytes from Rag-/- donors, bearing all activating Fc-receptors, into FcγRxRag-/- mice several days after immune serum treatment resulted in reduced viral titers in the recipient animals compared to the FcγRxRag-/- control mice. These results suggest an important role of monocytes in antibody mediated protection from MCMV infection. Keywords: Fc receptors, viral infection, NK cells, Monocytes, Antibodies, Viral Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Adaptive Immunity Citation: Bootz A, Winkler T and Mach M (2013). Monocytes rather than NK-cells contribute to antibody mediated protection from MCMV infection. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00918 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 28 Jun 2013; Published Online: 22 Aug 2013. * Correspondence: Mrs. Anna Bootz, Institute for Clinical and Molecular Virology, Friedrich-Alexander university Erlangen-Nürnberg,, Erlangen, Germany, anna.bootz@viro.med.uni-erlangen.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Anna Bootz Thomas Winkler Michael Mach Google Anna Bootz Thomas Winkler Michael Mach Google Scholar Anna Bootz Thomas Winkler Michael Mach PubMed Anna Bootz Thomas Winkler Michael Mach Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.