Vector transmission regulates immune control of Plasmodium virulence

Spence, P.J. et al. Nature 498, 228–231 (2013)

The authors show that transmission of the malaria parasite Plasmodium chabaudi chabaudi through its mosquito vector modifies the asexual blood-stage parasite, thus altering host immune responses to Plasmodium and parasite virulence.

The perivascular niche regulates breast tumour dormancy

Ghajar, C.M. et al. Nat. Cell. Biol. http://dx.doi.org/10.1038/ncb2767 (2 June)

This study provides new insights into how disseminated tumor cells are kept dormant by showing that in stable microvessels endothelial-derived thrombospondin-1 (TSP1) maintains breast cancer cells in a quiescent state. In sprouting vessels, TSP1 expression decreases, relieving this suppression and stimulating the growth of metastases.

High-density genotyping study identifies four new susceptibility loci for atopic dermatitis

Ellinghaus, D. et al. Nat. Genet. http://dx.doi.org/10.1038/ng.2642 (2 June)

By performing high-density genotyping in thousands of cases and controls, the authors identify four new susceptibility loci for the inflammatory skin disease atopic dermatitis, bringing the total of atopic dermatitis risk loci in European populations to 11.

Nucleation of platelets with blood-borne pathogens on Kupffer cells precedes other innate immunity and contributes to bacterial clearance

Wong, C.H.Y. et al. Nat. Immunol. http://dx.doi.org/10.1038/ni.2631 (16 June)

The authors show that platelets collaborate with specialized macrophages called Kupffer cells to clear bacteria. This mechanism occurred before recruitment of other innate immune cells and was needed for survival of the mouse host after bacterial infection.

Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor

Lyst, M.J. et al. Nat. Neurosci. http://dx.doi.org/10.1038/nn.3434 (16 June)

The authors identify a new mutational cluster in MeCP2, showing that Rett syndrome mutations in this region prevent the interaction of MeCP2 with the co-repressor complex NCoR/SMRT. Mice with a common Rett syndrome mutation in this domain had severe Rett-like phenotypes.