Dendritic cells (DCs) play an important role in both immunological tolerance and immunity as well as in pro- and anti-inflammatory responses. Upon uptake of apoptotic cells and apoptotic bodies, DCs degrade self antigens from them and induce anti-inflammatory response and T regulatory (Treg) cells resulting in the maintenance of tolerance to self antigens. Ageing is characterized by progressive immunodeficiency, inflammation, and autoimmunity. In this paper we will review the role of DCs in inflammation and autoimmunity in human ageing and will highlight the observations that DCs from aged humans display impairment in their capacity to uptake apoptotic cells, and paradoxically induce proinflammatory response and increased reactivity to self antigen (DNA). DNA from aged is hypomethylated and hypomethylation is associated with increased immunogenecity of self DNA.

Background: Colorectal cancer (CRC) screening is effective but underutilized. Although physician recommendation is an important predictor of screening, considerable variation in CRC screening completion remains. Purpose: To characterize the influence of patient trust in care providers on CRC screening behavior. Methods: Data were collected as part of a cluster-randomized CRC screening intervention trial performed in the San Francisco Community Health Network from March 2007 to January 2012 (analysis, Spring 2012). All study participants received a recommendation to complete CRC screening from their primary care provider (PCP). Included participants were aged 50-79 years, not current with screening, and completed the Wake Forest Trust Scale (WFTS) measuring trust in PCPs and doctors in general. Primary outcome was CRC screening completion (colonoscopy or fecal occult blood testing) within 12 months following enrollment. Multivariable association adjusted for race/ethnicity, language, and other sociodemographics was estimated using generalized estimating equations with logit link and binomial distribution. Results: WFTS response was 70.3% (701). Most participants (83%) were Latino, Asian, or black. Most had income <$30,000 (96%) and public health insurance (86%). Higher trust in PCP was associated with screening completion (OR=1.11, 95% CI=1.03, 1.17), but trust in doctors was not (OR=1.02, 95% CI=0.82, 1.28). Race, language, and other sociodemographic factors were not significant in multivariable analysis. Conclusions: After controlling for traditional factors, trust in PCP remained the only significant driver of CRC screening completion in low-income patients. Interventions to promote CRC screening may be improved by including efforts to enhance patient trust in PCP.

We have previously developed a daunorubicin resistant subline of Ehrlich ascites carcinoma (EA/DR) for studies on the reversal of daunorubicin resistance. The mean survival of untreated BALB/c mice bearing drug sensitive parental tumour (EA/DS) is 18.4 +/- 0.6 days, mice bearing EA/DS treated with five daily doses of 0.3 mg kg-1 daunorubicin greater than 60 days, and mice bearing EA/DR treated with the same daunorubicin regimen, 21.1 +/- 1.4 days. We now report complete reversal of daunorubicin resistance in EA/DR by cyclosporin A (CsA). The in vitro daunorubicin IC50, defined as that concentration of daunorubicin required to inhibit 50% of DNA synthesis, in EA/DR was 6.7 +/- 1.15 micrograms ml-1 compared to 2.8 +/- 0.72 micrograms ml-1 in EA/DS. This value was reduced to 2.8 +/- 0.52 and 2.1 +/- 0.10 micrograms ml-1 daunorubicin by 3.3 and 13.2 micrograms ml-1 CsA respectively, P less than 0.05. The MST of groups of host mice bearing EA/DR either untreated, treated with five daily doses of 0.3 mg kg-1 daunorubicin, treated with 80 mg kg-1 CsA in five divided daily doses or treated with combined daunorubicin-CsA were 19.0 +/- 1.0, 21.1 +/- 1.4, 24.0 +/- 2.6 and greater than 60 days respectively. The mean survival of groups of host mice bearing EA/DR treated with 5 mg kg-1 or 10 mg kg-1 CsA simultaneously with daunorubicin for five days was also greater than 60 days. These differences are highly significant.