Understanding How Stress Affects Humans Through The Study Of Social Stress That Molds The Monkey Immune System
If a monkey's social status changes, her immune system changes along with it say researchers who conducted the study with rhesus macaques at the Yerkes National Primate Research Center. This finding may have implications for how the stress of low socioeconomic status affects human health and how individuals' bodies adapt after a shift in their social environment. The results are published this week in the Proceedings of the National Academy of Sciences Early Edition. Researchers led by Jenny Tung, PhD, say they can predict a rhesus macaque's rank within a small group by examining gene expression levels in her immune cells. Tung, who was at the University of Chicago during the study, is now assistant professor of evolutionary anthropology at Duke University. Her colleagues and senior authors on the paper include Yoav Gilad, PhD, associate professor of human genetics at the University of Chicago, and Mark Wilson, PhD, chief of the Division of Developmental and Cognitive Neuroscience at Yerkes and director of the center's Biomarkers Core Laboratory.
Insulin is required for the regulation of blood sugar levels. In type I diabetes, the cells that produce insulin are destroyed by the immune system. Chantal Mathieu and colleagues at the University of Leuven have attempted to circumvent this response by taking advantage of the fact that the immune system accepts foreign gut bacteria. The Mathieu group engineered gut bacteria so that they produce a form of insulin, and asked if these bacteria could retrain the immune system in mice with type I diabetes to accept insulin-producing cells. They found that these special bacteria increased the frequency of cured mice when compared to traditional methods alone, with seemingly no undesirable effects. Traditional methods suppress the immune system, which brings with it unfavorable consequences such as increased infections.
Worries over vaccine risks can allow preventable contagious diseases, such as measles and whooping cough, to make a comeback. A new study, published in PLoS Computational Biology, shows how to predict ways in which population vaccinating behavior might unfold during a vaccine scare. "These findings might help in evaluating and developing global immunization programs and public health policy", said Professor Chris Bauch of the University of Guelph's Department of Mathematics and Statistics. Prof. Bauch and Samit Bhattacharyya of the University of Utah developed a mathematical, "Behavior-incidence" model based on game theory and social learning. They tested the model with real data from two infamous vaccine scares in England and Wales: the 1970s pertussis outbreak and the measles-mumps-rubella vaccine scare in the 1990s.
A new study led by Trinity College Dublin, in Ireland, finds that controlling or raising levels of the immune system component IL-18 in the retinas of patients with dry age-related macular degeneration (AMD), could prevent it progressing into the wet form of the disease. The researchers write about their findings in the 8 April online issue of Nature Medicine. AMD is the leading cause of central vision loss worldwide. Its advanced form makes every day life very difficult, preventing people from doing what many take for granted, such as read the paper, watch television, drive, use a computer, and see expressions on the faces of people they are in conversation with. A characteristic hallmark of AMD is having too many "drusen": yellowish-white deposits in the macula, the central region of the retina.
Individuals who suffer from autoimmune diseases also display a tendency to develop atherosclerosis - the condition popularly known as hardening of the arteries. Clinical researchers at LMU, in collaboration with colleagues in WÃ rzburg, have now discovered a mechanism which helps to explain the connection between the two types of disorder. The link is provided by a specific class of immune cells called plasmacytoid dendritic cells (pDCs). pDCs respond to DNA released from damaged and dying cells by secreting interferon proteins which stimulate the immune reactions that underlie autoimmune diseases. The new study shows that stimulation of pDCs by a specific DNA-protein complex contributes to the progression of atherosclerosis. The findings may have implications for new strategies for the treatment of a whole spectrum of conditions that are associated with chronic inflammatory reactions.