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The role of T cells in modulating the course of influenza infection in humans is not clear. Wilkinson et al. now report that, in the absence of strain-specific humoral immunity, preexisting cytotoxic CD4+ T cells limit the severity and duration of symptoms in humans challenged with influenza virus and suggest these CD4+ T cell responses might be harnessed in vaccine development.
The ability of Mycobacterium leprae to upregulate miRNA-21 provides an effective mechanism for the pathogen to escape from the vitamin D–dependent antimicrobial pathway.
Noise-induced hearing loss (NIHL) is a prevalent problem in the industrialized world. Now, Lukas Rüttiger and colleagues show that the phosphodiesterase inhibitor vardenafil can prevent NIHL in rats and mice.
Protective T helper 2 (TH2)-type responses are induced by parasite infection and can control inflammation and induce parasite expulsion. In this issue, Chen et al. report that in a mouse model of helminth infection, TH2-type responses protect against acute lung tissue damage by both suppressing inflammation and promoting macrophage-associated wound healing.
Cidea is typically thought of as a lipid droplet–associated cytoplasmic protein in brown adipose tissue. Peng Li and colleagues now show that it is also in the nucleus, and in mammary gland epithelial cells it acts as an essential transcriptional coactivator of C/EBPβ to regulate the expression of genes involved in milk lipid secretion during lactation.
The authors identify a new tumor suppressor role for Smurf2 that is linked to its regulation of histone modifications through RNF20. In the absence of Smurf2 in mice, and potentially also when its nuclear function is compromised in human tumors, higher levels of histone ubiquitination lead to a relaxation of chromatin structure, and alterations in DNA repair result in compromised genomic instability and increased tumorigenesis in aging mice. The findings suggest that loss of Smurf2 function may underlie tumor initiation by reshaping the epigenetic landscape of cells.
Mutations in the type I ryanodine receptor (RYR1), a calcium channel, leads to stimulus-induced pathological muscle contractions, including malignant hyperthermia. Currently there are no pharmacological agents to protect against this condition, but Susan Hamilton and her colleagues have now identified AICAR as one possible candidate compound. To date, AICAR has been thought to be an AMPK activator, but her group shows that in a mouse model of malignant hyperthermia it does not target this kinase, but rather RYR1, to prevent improper calcium leakage and pathology.
