Asthmatics have heightened antibody responses to rhinovirus although those specific for rhinovirus C are lower than responses specific for rhinovirus A suggesting poor immunity to this species.
To ascertain and compare T-cell memory responses induced by RV-A and RV-C in asthmatic and non-asthmatic children.
Peripheral blood mononuclear cells from 17 asthmatic children and 19 non-asthmatic controls were stimulated in vitro with peptide formulations to induce representative species-specific responses to RV-A and RV-C. Molecular profiling (RNA-Seq) was used to identify enriched pathways and upstream regulators.
Responses to RV-A showed higher expression of IFNG and STAT1 compared to RV-C and significant expression of CXCL9, 10 and 11 not found for RV-C. There was no reciprocal increase of Th2 cytokine genes or the Th2 chemokine genes CCL11, CCL17 and CCL22. RV-C induced higher expression of CCL24 (eotaxin-2) than RV-A in the responses of both non-asthmatic and asthmatics. Upstream regulator analysis showed both RV-A and, although to a lesser extent, RV-C induced predominant Th1 and inflammatory cytokine expression. The responses of asthmatics compared to non-asthmatics were lower for both RV-A and RV-C while retaining the pattern of gene expression and upstream regulators characteristic of each species. All groups showed activation of the IL-17A pathway.
RV-C induced memory cells with a lower IFN-γ type response than RV-A without Th2 upregulation. Asthmatics had lower recall responses than non-asthmatics while largely retaining the same gene activation profile for each species. RV-A and RV-C therefore induce qualitatively different T-cell responses.