Cholecystokinin2 Receptors

* and ** indicate p < 0

* and ** indicate p < 0.05 and p < 0.01 respectively. IL-12 directly antagonizes IL-13-induced gene manifestation Our observation that enhanced IL-12 production was associated with diminished AHR and mucus secretion, but unaltered production of IL-4, IL-5, IL-13 and IL-17A suggests that IL-12 may be regulating the severity of AHR by directly antagonizing signaling initiated by Th2 cytokines. assessed by circulation cytometry. n = 8 mice Ruboxistaurin (LY333531) from 2 self-employed experiments. Mean + SEM demonstrated. NIHMS426099-supplement-S2.eps (444K) GUID:?7F00DFDA-DDF5-4163-A354-3ADB6067491C S3: Supplementary Number 3: PD-L2 blockade does not enhance IL-12 p40 levels in BAL. A/J mice were treated with PBS or HDM intratracheally on days 0 and 14, and 250 g of rat IgG2a control (Iso) or anti-PD-L2 (PD-L2) intraperitoneally on days 0, 2, 14 and 16, and mice were sacrificed on day time 17. BAL was performed, and levels of IL-12 p40 were assessed by ELISA. MEAN + SEM demonstrated. n = 10 mice from 2 self-employed experiments. NIHMS426099-supplement-S3.eps (429K) GUID:?CDC8AD7E-70B4-4DE6-87B6-B4406C6FFA32 S4: Supplementary Number 4: PD-L2 or IL-12 blockade does not alter baseline tracheal pressure. A/J mice were treated with PBS or HDM intratracheally on days 0 and 14. Mice were given 250 g of rat IgG2a Ruboxistaurin (LY333531) control (Iso) or anti-PD-L2 (PD-L2) intraperitoneally on days 0, 2, 14 and 16 and/or 1 mg of rat IgG2a control (Iso) or anti-IL-12 (IL-12) intraperitoneally on days ?2 and 12. Mice were sacrificed on day time 17 for assessment of baseline AHR from the APTI method. Tracheal pressure was monitored for 1 minute prior to injection of intravenous acetylcholine. n = 10 mice from 2 self-employed experiments. Mean + SEM demonstrated. NIHMS426099-supplement-S4.eps (438K) GUID:?87BAC5DF-DE37-4B29-9FA1-535DD3783D15 S5: Supplementary Figure 5: Changes in AHR observed in mice received PD-L2 blocking and/or IL-12 blocking mAbs are not Ly6a associated with changes in local changes in cytokine mRNA levels. A/J mice were treated with PBS or HDM intratracheally on days 0 and 14. Mice were given 250 g of rat IgG2a control (Iso) or anti-PD-L2 (PD-L2) intraperitoneally on days 0, 2, 14 and 16 and/or 1 mg of rat IgG2a control (Iso) or anti-IL-12 (IL-12) intraperitoneally on days ?2 and 12. Mice were sacrificed on day time 17 and mRNA was isolated from snap-frozen lung samples for analysis of (A) IL-5 and (B) IL-13 manifestation by RT-PCR. n = 10 mice from 2 self-employed experiments. Mean + SEM demonstrated. NIHMS426099-supplement-S5.eps (464K) GUID:?87414132-E3B3-4489-A809-CDEC92ED8BE9 S6: Supplementary Figure 6: IL-12 and IFN inhibits IL-13-driven gene expression, and IL-13 inhibits IFN, but not IL-12-driven gene expression. (A) BMDCs were cultured in the presence of medium, IL-12, IL-13, or IL-12 + IL-13 (all at 10 ng/ml) for 18 hours. mRNA was harvested from your cells and manifestation of IFN, a Ruboxistaurin (LY333531) representative IL-12-induced gene, was examined by RT-PCR. (B) BMDCs were cultured in the presence of medium, IFN, IL-13, or IFN + IL-13 (all at 10 ng/ml) for 18 hours. mRNA was harvested from your cells and manifestation of IL-13-driven genes (Fizz1, Arg1, CD206) and IFN-driven genes (PD-L1) was examined by RT-PCR. (C) BMDCs were cultured in the presence of IL-13, IL-12 + IL-13 (all at 10 ng/ml), or IL-12 + IL-13 + IFN (at 5 g/ml) for 18 hours. mRNA was harvested from your cells and manifestation of IL-13-driven genes was examined by RT-PCR. *** and * indicate p < 0.001 and p < 0.5 respectively. n = 4 replicates for each condition tested. 1 experiment of 2 performed demonstrated. NIHMS426099-supplement-S6.eps (626K) GUID:?C3C34B1B-83A4-4F31-8A43-0693189C4936 Abstract Studies examining the role of PD-L2/PD-1 in asthma have yielded conflicting results. To clarify its part, we examined PD-L2 manifestation in biopsies from human being asthmatics and lungs of aeroallergen-treated mice. PD-L2 manifestation in bronchial biopsies correlated with the severity of asthma. In mice, allergen exposure increased PD-L2 manifestation on pulmonary myeloid dendritic cells, and PD-L2 blockade diminished allergen-induced airway hyperresponsiveness (AHR). In contrast, PD-1 blockade experienced no impact, suggesting that.