title: Human major group rhinoviruses downmodulate the accessory function of monocytes by inducing IL-10.
abstract: Human rhinoviruses (HRVs) are the predominant cause of the common cold. Although this disease is per se rather harmless, HRV infection is considered to set the stage for more dangerous pathogens in vivo. Here we demonstrate that HRV-14, a member of the major group HRV family, can efficiently inhibit antigen-induced T-cell proliferation and T-cell responses to allogeneic monocytes. HRV-14 triggered a significant downregulation of MHC class II molecules on monocytes. Moreover, supernatants from monocytes cultured in the presence of HRV-14 strongly reduced the allogeneic T-cell stimulatory property of untreated monocytes and monocyte-derived dendritic cells (md-DCs), whereas Epstein Barr virus-transformed B-lymphoblastoid cells were not sensitive. Analysis of the supernatant revealed that HRV-14 induced the production of significant amounts of the immunosuppressive cytokine IL-10. The important T-cell stimulatory cytokine IL-12 or the proinflammatory cytokines IL-1beta or TNF-alpha were not detected or were only minimally detected. Finally, monocytes pretreated with HRV-14 were greatly inhibited in their production of IL-12 upon stimulation with IFN-gamma/LPS. These observations suggest that altered cytokine production in mononuclear phagocytes upon interaction with HRV downmodulates appropriate immune responses during the viral infection.
authors.affiliation: Institute of Immunology, and Institute of Biochemistry, University of Vienna, A-1090 Vienna, Austria. Johannes.Stoeckle@univie.ac.at
authors.forename: J
authors.initials: J
authors.lastname: Stöckl
authors.forename: H
authors.initials: H
authors.lastname: Vetr
authors.forename: O
authors.initials: O
authors.lastname: Majdic
authors.forename: G
authors.initials: G
authors.lastname: Zlabinger
authors.forename: E
authors.initials: E
authors.lastname: Kuechler
authors.forename: W
authors.initials: W
authors.lastname: Knapp
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D002478:Cells, Cultured; D004768:Enterotoxins / Q000276:immunology; D005786:Gene Expression Regulation / Q000276:immunology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D006367:HeLa Cells; D006801:Humans; D007375:Interleukin-1 / Q000032:analysis; D016753:Interleukin-10 / Q000096:biosynthesis / Q000235:genetics*; D015847:Interleukin-4 / Q000494:pharmacology; D007700:Kinetics; D008213:Lymphocyte Activation / Q000187:drug effects; D009000:Monocytes / Q000276:immunology* / Q000821:virology*; D016853:Muromonab-CD3 / Q000494:pharmacology; D011994:Recombinant Proteins / Q000494:pharmacology; D012229:Rhinovirus / Q000276:immunology*; D013211:Staphylococcus aureus; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D013745:Tetanus Toxoid / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015703:Antigens, CD; D004768:Enterotoxins; D007375:Interleukin-1; D016853:Muromonab-CD3; D011994:Recombinant Proteins; D013745:Tetanus Toxoid; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015847:Interleukin-4; C026066:enterotoxin A, Staphylococcal; C031818:enterotoxin B, staphylococcal; D016178:Granulocyte-Macrophage Colony-Stimulating Factor