Student Subjectivity in the Marketised University

We present data from an exploratory qualitative interview-based pedagogical research project on the development of student agency in higher education. Our aim was to respond to Nick Zepke’s claim that what is often missing from the current neoliberal discourse of higher education ‘is students having a voice in what and how they learn and how they can action their voice in the wider community as agentic citizens.’ Informed by Lacanian discourse analysis, our project investigated the opportunities and threats facing some of our undergraduate students as they struggled to exercise agency and develop autonomy in the marketised university. Repeat interviews (n = 15) with final year students focussed on the psychosocial categories of power, affect, intersubjectivity and desire. The analysis was guided by Lacan’s theory of the four discourses, an account of the vicissitudes of agency. We found that students can move between discourses depending on the extent to which their agency (operationalised here as Lacan’s ‘object cause of desire,’ the objet petit a) was enabled or thwarted. Our critique of the metaphor of the ‘student journey’ addresses the implications for learning and teaching and the university’s mission to develop its students in light of perceived commercial pressures

Critical Roles for LIGHT and Its Receptors in Generating T Cell-Mediated Immunity during Leishmania donovani Infection

LIGHT (TNFSF14) is a member of the TNF superfamily involved in inflammation and defence against infection. LIGHT signals via two cell-bound receptors; herpes virus entry mediator (HVEM) and lymphotoxin-beta receptor (LTβR). We found that LIGHT is critical for control of hepatic parasite growth in mice with visceral leishmaniasis (VL) caused by infection with the protozoan parasite Leishmania donovani. LIGHT-HVEM signalling is essential for early dendritic cell IL-12/IL-23p40 production, and the generation of IFNγ- and TNF-producing T cells that control hepatic infection. However, we also discovered that LIGHT-LTβR interactions suppress anti-parasitic immunity in the liver in the first 7 days of infection by mechanisms that restrict both CD4+ T cell function and TNF-dependent microbicidal mechanisms. Thus, we have identified distinct roles for LIGHT in infection, and show that manipulation of interactions between LIGHT and its receptors may be used for therapeutic advantage

Constructing the Suspect: A Brief History of the Lie Detector

If you can’t trust the machine, who or what can you trust

IL-17A-Producing gamma delta T Cells Suppress Early Control of Parasite Growth by Monocytes in the Liver

Intracellular infections, such as those caused by the protozoan parasite Leishmania donovani, a causative agent of visceral leishmaniasis (VL), require a potent host proinflammatory response for control. IL-17 has emerged as an important proinflammatory cytokine required for limiting growth of both extracellular and intracellular pathogens. However, there are conflicting reports on the exact roles for IL-17 during parasitic infections and limited knowledge about cellular sources and the immune pathways it modulates. We examined the role of IL-17 in an experimental model of VL caused by infection of C57BL/6 mice with L. donovani and identified an early suppressive role for IL-17 in the liver that limited control of parasite growth. IL-17–producing γδ T cells recruited to the liver in the first week of infection were the critical source of IL-17 in this model, and CCR2+ inflammatory monocytes were an important target for the suppressive effects of IL-17. Improved parasite control was independent of NO generation, but associated with maintenance of superoxide dismutase mRNA expression in the absence of IL-17 in the liver. Thus, we have identified a novel inhibitory function for IL-17 in parasitic infection, and our results demonstrate important interactions among γδ T cells, monocytes, and infected macrophages in the liver that can determine the outcome of parasitic infection