or example, in rye seeds stored at 40uC with 10% MC nucleic acid degradation resulted in randomly sized DNA fragments, whilst at 14% MC DNA fragments of around 160 base pairs, characteristic of inter-nucleosomal cleavage associated with PCD, were observed. Long term studies to dissect the ageing process at lower temperatures and RH, such as the conditions used for ex situ seed storage may enable the elucidation of molecular markers that could be used to diagnose seed deterioration prior to viability loss, which would be a valuable tool for seed conservation and agriculture. In addition, large scale investigations which combine transcriptomic, proteomic and metabolomic data are necessary to provide the missing pieces in the seed ageing puzzle. 11 Transcriptome Analysis of Pea Seed Ageing The IL-12 cytokine superfamily member IL-27 is an important 9405293 regulator of pro-inflammatory immune responses. Increased numbers of effector CD4+ T cells are found in the livers of IL-27R deficient mice during Plasmodium berghei NK65, Toxoplasma gondii, Leishmania donovani and Trypanasoma 23033494 cruzi infections, in the lungs of WSX-12/2 mice during Mycobacterium tuberculosis infection and in the intestine of WSX-12/2 mice during Trichuris muris infection. The mechanisms through which IL27 limits Th1, Th2 and Th17 responses, enhances CD4+ T cell IL10 production and regulates the polarisation of Foxp3+ regulatory T cells, have been widely studied. By contrast, the pathways by which IL-27 inhibits effector T cell purchase Regadenoson accumulation in nonlymphoid tissues during infection are poorly understood, but may include limiting CD4+ T cell proliferation or enhancing cellular apoptosis in situ. In support of these theories, CD4+ T cells from WSX-12/2 mice are hyper proliferative following in vitro stimulation with antiCD3/CD28 and proliferate more extensively in the lungs of WSX-12/2 mice than WT mice during Mycobacterium tuberculosis infection. Whilst the role of IL-27 in controlling T cell apoptosis has not been directly examined, IL-6 and IL-12 are both known to exert anti-apoptotic effects on CD4+ T cells and concentrations of both these cytokines are significantly increased in WSX-12/2 mice during infection. Alternatively, IL-27 might limit the autonomous chemotactic activity of CD4+ T cells, and/or affect the expression of liver derived chemotactic/ migratory factors. In support of this latter hypothesis, we have shown that splenic CD4+ T cells from malaria-infected WSX-12/ 2 mice express higher levels of CCR5 than cells from WT mice and are consequently hyper responsive to CCR1 and CCR5 ligands. WSX-1 Limits Intrahepatic CD4+ T Cell Responses In this study we have used Plasmodium berghei NK65 as a model systemic infection, to investigate the pathways by which IL-27 restricts effector CD4+ T cell accumulation in the liver during inflammation. We demonstrate that intrahepatic CD4+ T cell proliferation and apoptosis are unaffected by the absence of WSX1 signalling. Instead our results show that IL-27 attenuates CD4+ T cell accumulation in the liver by inhibiting T cell migratory pathways. Surprisingly, we find that CD4+ T cell accumulation in the livers of infected WSX-12/2 mice is not orchestrated by nonclassical chemokine pathways. Rather, increased CD4+ T cell migration in infected WSX-12/2 mice seems to result from the loss of IL-27-mediated suppression of Th1 differentiation and chemotaxis. We conclude that IL-27 restricts the accumulation of pathogenic T cells in the live