However, although IL-2 induced a similar pattern of STAT5 phosphorylation, the proliferative response of CD4+ T cells and the expression of FOXP3+ remained significantly lower in RSV-infected infants.
The current studies demonstrated differences in PBMC responses to the two viruses very early after exposure, including reduced fos protein and CD69 expression and IL-2 production by RSV-exposed T lymphocytes.
Coculture of adult RSV-infected DCs with autologous T cells induced secretion of gamma interferon (IFN-γ), interleukin 12p70 (IL-12p70), IL-2, and tumor necrosis factor alpha (TNF-α).
Patients hospitalized because of RSV infection had increased numbers of CD16(+) and CD56(bright) cells and had RSV-specific increases in Th1 (interleukin [IL]-2 and interferon-gamma) and Th2 (IL-4 and IL-6) cytokines and CC chemokines (macrophage inflammatory protein [MIP]-1alpha, MIP-1beta, and RANTES [regulated on activation, normally T cell expressed and secreted]) mRNA expression.
Serum IL-2 was not detectable in mice treated with Ad-pRSV-IL-2, whereas expression peaked at a total of 1--2 ng at 24 hours but declined very rapidly in the Ad-pCMV-IL-2-treated group.
Analysis of total pulmonary cytokine mRNA isolated 1 and 4 days following infection with rRSV/mIL-2 revealed elevated levels of mRNA for IL-2, gamma interferon (IFN-gamma), IL-4, IL-5, IL-6, IL-10, IL-13, and IL-12 p40 compared to those for wt rRSV.
The production of IFN-gamma, IL-2, -4, -5 and -10 cytokine mRNA by RT-PCR and intracellular cytokines by flow cytometry following RSV challenge of vaccinated mice were therefore compared.