In conclusion, this study revealed that nurses' influenza vaccination behaviours are complex. Knowledge and risk perception were identified as two predictors influencing nurses' vaccination decisions with the health belief pattern of 'less powerful others ' being an important predictor in the never vaccinated ; however, there are other influential factors which need to be identified in future studies. IFN-γ Signaling to Astrocytes Protects from Autoimmune Mediated Neurological Disability Demyelination and axonal degeneration are determinants of progressive neurological disability in patients with multiple sclerosis (MS). Cells resident within the central nervous system (CNS) are active participants in development, progression and subsequent control of autoimmune disease; however, their individual contributions are not well understood. Astrocytes, the most abundant CNS cell type, are highly sensitive to environmental cues and are implicated in both detrimental and protective outcomes during autoimmune demyelination. Experimental autoimmune encephalomyelitis (EAE) was induced in transgenic mice expressing signaling defective dominant-negative interferon gamma (IFN-γ) receptors on astrocytes to determine the influence of inflammation on astrocyte activity. Inhibition of IFN-γ signaling to astrocytes did not influence disease incidence, onset, initial progression of symptoms, blood brain barrier (BBB) integrity or the composition of the acute CNS inflammatory response. Nevertheless, increased demyelination at peak acute disease in the absence of IFN-γ signaling to astrocytes correlated with sustained clinical symptoms. Following peak disease, diminished clinical remission, increased mortality and sustained astrocyte activation within the gray matter demonstrate a critical role of IFN-γ signaling to astrocytes in neuroprotection. Diminished disease remission was associated with escalating demyelination, axonal degeneration and sustained inflammation. The CNS infiltrating leukocyte composition was not altered; however, decreased IL-10 and IL-27 correlated with sustained disease. These data indicate that astrocytes play a critical role in limiting CNS autoimmune disease dependent upon a neuroprotective signaling pathway mediated by engagement of IFN-γ receptors. CNS resident cells are targets of autoimmune mediated damage but also active participants in disease development, progression and control [1, 2] . However, their contributions to neuroprotection and regulation by inflammatory mediators are not well defined. CNS insults, including autoimmune disease, initiate rapid astrocyte activation characterized by cellular hypertrophy and increased intermediate filament glial fibrillary acidic protein (GFAP) expression [3] [4] [5] . Astrocytes form a physical barrier surrounding areas of inflammation initially limiting bystander tissue damage [6, 7] . However, this barrier subsequently impedes axonal regeneration contributing to sustained disability [3, 5, 8] . Innate and adaptive pro-inflammatory astrocyte functions include production of pro-inflammatory cytokines, reactive oxygen species, chemokines, and matrix metalloproteinases [3] [4] [5] . By contrast, secretion of anti-inflammatory cytokines and scavengers of reactive oxygen species, as well as inhibition of both microglial activation and tumor necrosis factor (TNF) secretion, all support an astrocyte mediated anti-inflammatory function [3] [4] [5] . Therefore, astrocyte activation constitutes a ubiquitous, yet heteroge-neous response associated with both promoting and inhibiting CNS repair [3] [4] [5] .