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Updated: May 6, 2026
An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 11, 2013
Human major group rhinoviruses downmodulate the accessory function of monocytes by inducing IL-10
1Institute of Immunology, and Institute of Biochemistry, University of Vienna, A-1090 Vienna, Austria. Johannes.Stoeckle@univie.ac.at
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.
Insights
Human rhinovirus (HRV) infection suppresses immune responses by reducing T-cell proliferation and downregulating MHC class II on monocytes. This leads to increased IL-10 production, hindering effective immune cell communication.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human rhinoviruses (HRVs) are the primary cause of the common cold.
- HRV infections can predispose individuals to secondary, more severe infections.
Purpose of the Study:
- To investigate the impact of HRV-14 on T-cell responses and monocyte function.
- To elucidate the mechanisms by which HRV-14 modulates immune cell interactions.
Main Methods:
- Antigen-induced T-cell proliferation assays.
- Analysis of MHC class II expression on monocytes.
- Cytokine profiling (IL-10, IL-12, IL-1β, TNF-α) in monocyte cultures.
- Assessment of monocyte-derived dendritic cells (md-DCs) and B-lymphoblastoid cells' sensitivity.
Main Results:
- HRV-14 significantly inhibited antigen-induced T-cell proliferation and allogeneic monocyte responses.
- HRV-14 induced downregulation of MHC class II molecules on monocytes.
- Supernatants from HRV-14-treated monocytes suppressed T-cell stimulation by monocytes and md-DCs.
- HRV-14 promoted significant IL-10 production while suppressing IL-12, IL-1β, and TNF-α.
- Monocyte IL-12 production was inhibited upon stimulation with IFN-γ/LPS after HRV-14 pretreatment.
Conclusions:
- HRV-14 impairs T-cell responses and alters monocyte immunophenotype and function.
- HRV-14-induced immunosuppression is mediated, in part, by increased IL-10 production.
- These findings suggest HRV infection can dysregulate mononuclear phagocyte cytokine production, downmodulating immune responses.
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