Synergistically with IL-12, IL-18 could induce interferon-γ production from T, B and natural killer cells (6).
Human IL-32 recombinant protein has been utilized in mice [ 18, 29], and so we determined whether IL-32 could induce IL-17 production in an autoimmune arthritis mouse model.
Furthermore, it was previously shown that the combination of IL-2 and IL-21 could induce additional effects on the enhancement of ADCC activity (Skak et al, 2008a).
In this study, we investigated whether in IVD degeneration there is local production of the cytokine IL-1 and whether IL-1 could induce the cellular changes characteristic of IVD degeneration.
Upon identifying the ability of IL-27 to induce BST-2 expression, we decided to investigate whether IL-6 could induce BST-2 in the same way as IL-27, since both cytokines signal via gp130 to activate STAT327.
Our data demonstrated that A. baumannii LPS stimulates airway epithelial cells to secrete IL-8 thereby suggesting that this LPS-elicited IL-8 could induce a pulmonary influx of neutrophils.
As shown in Figure 3, IL-27 could induce significantly higher release of inflammatory chemokine CCL2, CXCL9 and CXCL10 from RA-FLS than that of control FLS (all P < 0.05).
Supporting this idea, IL-21 induced in vitro proliferation in the presence of cytokines such as IL-7 and IL-15, and could induce modest amounts of proliferation on its own [16], [39], [40].
IL-32 and IL-17 also could induce resorption by osteoclasts in a RANKL-dependent manner.
A decade ago it was assumed that IL-4 and TGF-β could induce IL-9 production from CD4+ T cells [ 29], and this theory was proved by two independent groups [ 9, 10].
