IFN-γ suppresses the accumulation of neutrophils.

<p>Animals were inoculated i.p. with 500 μg/mouse normal rat IgG (A) or anti-IFN-γ (B) at 1 hour prior to surgery. The animals were euthanized on day 3 post-surgery, the NPCs were isolated, and the neutrophils were stained (Ly-6G/CD11b) and quantified by flow cytometry. A summary of experimental results is presented in the table. Data are derived from a single experiment representative of two independent experiments, n  =  3-6 mice/group.</p

Kupffer cells induce the activation and accumulation of iNKT cell in biliary obstructed livers.

<p>Animals were treated with Cl₂MDP-L to deplete Kupffer cells prior to BDL; control mice received PBS. At 18 hours post-BDL, the NPCs were teased through screens, counted, purified on Percoll gradients and stained. Hepatic, CD1d-tetramer⁺ iNKT cells were quantified (A), and the expression of CD25 (B), CD69 (C), and ICAM-1 (D) was determined by flow cytometry. Values in parentheses denote percentages of expression. A summary of experimental results is presented in table format containing cell numbers and statistical analyses. Data are derived from three independent experiments, n  =  3-6 mice/group. n/a  =  not available; small sample size precludes statistical analysis.</p

Liver injury is significantly increased in the absence of iNKT cells.

<p>Plasma ALT (A) and AST (B) levels were determined in iNKT cell-deficient and WT mice at three days post-BDL. Representative liver sections were collected from the WT (C) and iNKT^−/− (D) mice, embedded in paraffin, sectioned, stained with Hematoxylin & Eosin, and scored. The livers of BDL iNKT^−/− mice exhibited significantly greater areas of necrosis (indicated by black arrows) (E). Data are derived from four independent experiments, n  =  3-5 mice/group. *Significantly greater than sham-operated controls, <i>P</i> <0.05; **Significantly greater than BDL, WT mice, <i>P</i> <0.05 (Student’s <i>t</i>-test).</p

LFA-1-dependent activation and accumulation of iNKT cells in cholestatic livers.

<p>BDL WT mice were treated with anti-LFA-1 monoclonal antibody or normal rat IgG at 1 hour prior to BDL. Animals were euthanized at 18 hours post-surgery, the NPC were purified on a Percoll gradient, and the iNKT cell markers were stained. CD1d-tetramer⁺ iNKT cells were quantified (A) and CD25 expression was determined (B) by flow cytometry. Values in parentheses denote percentages of expression. A summary of experimental results is presented in table format containing cell numbers and statistical analyses. Data are derived from three independent experiments, n = 3-6 mice/group.</p

Distribution frequency of the <i>IκB</i> haplotype in controls and hepatocellular carcinoma patients.

<p>OR, odds ratio; CI confidence interval.</p

Clinical status and <i>NF-κB</i> genotypic frequencies in 135 hepatocellular carcinoma (HCC) patients.

<p>>T2: multiple tumor of >5 cm or tumor involving a major branch of the portal or hepatic veins.</p>a<p>The AORs with their 95% CIs were estimated by multiple logistic regression models after controlling for age, gender, smoking and drinking.</p>b<p>The AORs with their 95% CIs were estimated by multiple logistic regression models after controlling for age, gender, smoking and drinking.</p>*<p><i>P</i> value <0.05 as statistically significant.</p

Distributions of demographic characteristics in the 520 controls and 135 patients with hepatocellular carcinoma.

<p>Mann-Whitney U test or Fisher’s exact test was used between healthy controls and patients with HCC.</p>*<p><i>p</i><0.05 which was statistically significant.</p

Association of the nuclear factor (NF)-κB and inhibitor of NF-κB (IκB) genotypic frequencies with the hepatocellular carcinoma laboratory status.

<p>Association of the nuclear factor (NF)-κB and inhibitor of NF-κB (IκB) genotypic frequencies with the hepatocellular carcinoma laboratory status.</p

NF-κB inhibitor effect on lipopolysaccharide-induced monocyte chemoattractant protein-1 and osteopontin expression in NZB/W mesangial cells

<p><b>Copyright information:</b></p><p>Taken from "Mesangial cells of lupus-prone mice are sensitive to chemokine production"</p><p>http://arthritis-research.com/content/9/4/R67</p><p>Arthritis Research & Therapy 2007;9(4):R67-R67.</p><p>Published online 7 Jul 2007</p><p>PMCID:PMC2206365.</p><p></p> Growth-arrested (under 2% fetal bovine serum (FBS)) mesangial cells were preincubated for 2 hours with -tosyl-1-phenylalanine chloromethyl ketone (TPCK) or dexamethasone (Dex), and then 10 μg/ml lipopolysaccharide (LPS) was added for 12 hours: monocyte chemoattractant protein-1 (MCP-1) mRNA levels and osteopontin (OPN) mRNA levels were measured by real-time PCR analysis. Growth-arrested (under 2% FBS) mesangial cells were preincubated for 2 hours with TPCK or Dex, then 10 μg/ml LPS was added for 24 hours: MCP-1 protein levels in the supernatant were measured by ELISA, and OPN protein levels in the cell lysate were measured by western blot analysis; semiquantitative data are shown. The MCP-1 protein expression levels at various time points were normalized to total protein (pg/mg). The experiment was performed in triplicate, and results are expressed as the mean ± standard error. **< 0.01, ***< 0.005, = 6. White bar, absence of LPS; black bar, LPS alone; hatched bar, TPCK and LPS or Dex and LPS

Toll-like receptor 4 and myeloid differentiation factor 88 mRNA in NZB/W mesangial cells (lipopolysaccharide treatment)

<p><b>Copyright information:</b></p><p>Taken from "Mesangial cells of lupus-prone mice are sensitive to chemokine production"</p><p>http://arthritis-research.com/content/9/4/R67</p><p>Arthritis Research & Therapy 2007;9(4):R67-R67.</p><p>Published online 7 Jul 2007</p><p>PMCID:PMC2206365.</p><p></p> Growth-arrested (under 2% fetal bovine serum (FBS)) mesangial cells were incubated with 10 μg/ml lipopolysaccharide (LPS) for different periods of time, and then Toll-like receptor 4 (TLR-4) and myeloid differentiation factor 88 (MyD88) mRNA levels were measured by real-time PCR analysis. The experiment was performed in triplicate, and results are expressed as the mean ± standard error, = 6. The last time point without LPS stimulation (unstimulated) was presented as the negative control. *< 0.05, **< 0.01