However, it seems most likely that a difference in the immunising regime offers
the most plausible explanation. In the 1980s, 2000 T. circumcincta L3 were given to the previously infected sheep 5 days a week whereas in the recent series of trials this dose was administered only three times per week, i.e. the recent sheep received only 60% of the dose given in the 1980s. Exposure to the heavier immunising infection appeared to confer a more solid immunity to subsequent challenge in yearlings and yet make the lambs more susceptible (Table 2). There was no evidence from the recent PD-0332991 manufacturer trials with the lighter trickle infection to support the idea that one or more components of the immune response
were defective in lambs. This includes examination of the abomasal histology where for example mast cell numbers were in the normal range (data being prepared for publication). We therefore hypothesise that only older, more resilient sheep were able to respond adequately following the heavier trickle, whereas the growing lambs, being less able to cope with the pathological effect of the ALK activation greater parasite load, were only able to mount a weak, relatively ineffective response post-challenge. In conclusion, we suspect that age and acquired immunity in ovine gastrointestinal nematodiasis is more likely to be due to the lack of resilience to infection on the part of lambs than to a specific immunological deficiency. The authors would like to thank Frank Jackson’s laboratory at Moredun for supplying parasites, Stephen Smith and Andy Greer for technical assistance, Mara Rocchi for assistance with the FACS analysis and Jill Sales of BIOSS for statistical Amrubicin analysis. We would also like to thank Roy Davie, David Kennedy and Manus Graham for help with surgery. This work was funded by a Veterinary Training Research Initiative from the Department of Environment, Food and Rural Affairs and by the Scottish Government Rural and Environment Research and Analysis Directorate. “
“Mycobacterium
tuberculosis (TB) often causes persistent infection and many immune cell subsets and regulatory mechanisms may operate throughout the various stages of infection. We have studied dendritic cell (DC) subsets, regulatory T cells (Treg) and the expression of activation and apoptosis markers on CD4+ and CD8+ T cells in blood from patients with active TB (n = 20), subjects with positive QuantiFERON-TB GOLD (QFT) test (LTBI, latent TB infection) (n = 20) before and after 3 months of preventive anti-tuberculous therapy and from QFT-negative controls (n = 28). The frequency of CD4+CD25+CD127− Treg was highest in the group with active TB (P = 0.001), but also increased in the LTBI group (P = 0.006) compared to controls.