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The expression of antibodies to protect against an infectious disease can be achieved by the injection into the host of vectors carrying the gene to the relevant antibodies. Here the authors demonstrate the applicability of this technique to protection from HIV in a humanized mouse model, showing this to be a valid route to pursue in vaccine development for humans (pages 296–300).
Interferon-β (IFN-β) is widely used to treat multiple sclerosis (MS), but its mechanism of protection remains obscure. A new study shows that IFN-β induces FoxA1+ regulatory T cells, a new regulatory T cell population, which suppress conventional T cells via programmed cell death 1 ligand 1. This cell subset limits disease in a mouse model of MS and was found in patients with MS who responded to IFN-β therapy (pages 272–282).
Modification of a natural product with antibiotic properties to block its efflux from Mycobacterium tuberculosis results in a new drug candidate for tuberculosis with a promising therapeutic profile in mice (pages 152–158).
A new study in mice provides a link between dietary fiber intake, amounts of intestinal and systemic short-chain fatty acids, changes in the microbiome and allergic responses in the airways. The findings support the growing appreciation of a potential therapeutic role of diet in treating allergic diseases (pages 159–166).
Retinoic acid and arsenic trioxide cure individuals with acute promyelocytic leukemia (APL). In mouse models, these drugs eradicate tumor cells by activating the tumor suppressors p53 and PML to induce senescence of cancer cells (pages 167–174).
The concordant epidemics of asthma and obesity are both associated with inflammation, and obesity has been shown to be an independent risk factor for asthma. A new study in mice indicates that part of the immunological connection between obesity and asthma involves inflammasome activation and production of the cytokine interleukin-17 by innate lymphoid cells in the lung (pages 54–61).
Under most circumstances, Foxp3+ regulatory T (Treg) cells are a stable T cell population essential for maintaining self-tolerance. A study now shows that the inflammatory environment in autoimmune arthritis induces conversion of a subset of Foxp3+ T cells into interleukin-17–producing cells that contribute to disease pathogenesis (pages 62–68).
Many tumors display a hierarchical organization that is maintained by a self-renewing 'cancer stem cell' population. A new study in mice shows that targeting the self-renewal regulator BMI-1 abrogates the tumorigenic capacity of colon cancer stem cells, providing a new therapeutic strategy (pages 29–36).
Liver-stage Plasmodium infection triggers a type I interferon transcriptional program in hepatocytes that amplifies an innate immune response within hepatic myeloid cells. This minimizes liver parasite load and delays the release of disease-causing parasites into the bloodstream (pages 47–53).
