Copyright © 2011 Xiao-Qing Wei et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Candida albicans is an opportunistic fungal pathogen that normally exists as a harmless commensal in humans. In instances where host debilitation occurs, Candida can cause a range of clinical infections, and whilst these are primarily superficial, effecting mucosal membranes, systemic infections can develop in severely immunocompromised individuals. The mechanism of host immunity during commensal carriage of C. albicans has been intensively studied. In this paper, we present the most recent information concerning host recognition of C. albicans leading to cytokine production and the subsequent T-cell responses generated in response to C. albicans. Particular focus is given to the role of the IL-12 cytokine family including IL-12, IL-23, IL-27, and IL-35, in host immunity to Candida.CD4 + T-cells are considered crucial in the regulation of immunity and inflammation. In this regard, the role of Th1/2, helper cells, together with the recently identified Th17 and Treg cells in candidosis will be discussed. Understanding the detailed mechanisms that underlie host immunity to Candida not only will be of benefit in terms of the infections caused by this organism but could also be exploited in the development of therapeutic interventions for other diseases. 1.

Copyright © 2011 Anne-Marie Drolet et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Th17 cells have been implicated in a number of inflammatory and autoimmune diseases. The phospholipid mediator plateletactivating factor (PAF) is found in increased concentrations in inflammatory lesions and has been shown to induce IL-6 production. We investigated whether PAF could affect the development of Th17 cells. Picomolar concentrations of PAF induced IL-23, IL-6, and IL-1β expression in monocyte-derived Langerhans cells (LCs) and in keratinocytes. Moreover, when LC were pretreated with PAF and then cocultured with anti-CD3- and anti-CD28-activated T cells, the latter developed a Th17 phenotype, with a significant increase in the expression of the transcriptional regulator RORγt and enhanced expression of IL-17, IL-21, and IL-22. PAF-induced Th17 development was prevented by the PAF receptor antagonist WEB2086 and by neutralizing antibodies to IL-23 and IL-6R. This may constitute a previously unknown stimulus for the development and persistence of inflammatory processes that could be amenable to pharmacologic intervention. 1.

ii Johne’s disease (JD), caused by the pathogen Mycobacterium avium subspecies paratuberculosis (MAP), is a chronic inflammatory bowel disease of ruminants that is characterised in its clinical stage by progressive weight loss/wasting and profuse diarrhea. Immune responses to MAP infection are initially characterised by a Th1 T cell response that subsequently decreases over disease progression. Detection of MAP occurs via pathogen recognition receptors (PRR) including NOD2 and the toll like receptors (TLR). Mutations in NOD2 have been identified as a susceptibility factor to JD. To cause infection MAP has a documented role in manipulating its environment including gene expression profiles. The aims of this project was to map the NOD2 gene for mutations associated with resistance or susceptibility to JD in red deer (Cervus elaphus), and to investigate the gene expression profiles of deer of demonstrated resistance and susceptibility for informative factors in disease progression. Foundational work, carried out at AgResearch Invermay investigating the heritability