Impact of IL-33 on Th0 cell differentiation from naïve T cells.

<p>Naïve T-cells from buffy coats were differentiated into Th0 (n = 5) in the presence or absence of IL-33 (10 ng/ml) and thereafter subjected to intracellular cytokine staining. IL-33 promoted an increase in Th2-producing cells in four out of five experiments. There was no evidence of an IL-17 induction.</p

IFN-γ is a strong inducer of IL-33 in sinonasal epithelial cells.

<p>Primary sinus epithelial cells (CRS patient) were subjected to T-cell lineage specific or T-cell related cytokines or their combinations. mRNA expression of IL-33 was measured via real time RT-PCR. IFN-γ induced a relevant increase in IL-33 (A). The observed effects are independent of the source of HSEC cells (B; n = 5; mRNA levels are expressed as fold expression of the unstimulated control). The induction of IL-33 via IFNγ was dose dependent (C). The presence of the uncleaved form of IL-33 after co-culture of HSEC with 50 μg/ml IFNγ was confirmed by western blot (D). Only Th1 cells, but not Th2, Th9, Th17 or Treg were significantly up-regulated IL-33 mRNA expression in HSECS (E).</p

The interaction of IL-33 with Th1, Th2 and Th17 responses in chronic rhinosinusitis.

<p>IL-33 may act as an “alarmin” that is released by HSECS via a Th1 dependent mechanism. IL-33 itself induces IL-13 and IL-5 and thereby contributes to the limitation of both Th17- and Th1-related arms of the inflammation.</p

Sinus tissue from chronic rhinosinusitis patients shows a mixed pro-inflammatory cytokine profile.

<p>Whole sinus tissue mRNA from CRS patients (CRSsNP n = 16; CRSwNP n = 8) and controls (n = 8) of an array of cytokines and transcription factors was quantified by real time PCR (Mann Whitney U-Test; mean +/- SEM).</p