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Better tools are needed for detecting Mycobacterium tuberculosis and defining the dynamic interactions of M. tuberculosis with its human host.

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Sullivan et al. showed that pharmacological suppression of BET proteins by a highly selective brain-permeable inhibitor, results in the suppression of genes that have been linked to autism spectrum disorders in humans. BET inhibitor treatment of young mice led to the induction of an autism-like syndrome characterized by alterations in social behaviors. These findings suggest a key role of the BET-controlled gene networks in the development of ASD.

Type 3 lymphoid cells (ILC3s) are required for epithelial activation and proliferation in response to small intestinal tissue damage induced by chemotherapeutics. Multiple ILC3 subsets are activated after intestinal damage, and the absence of ILC3s or their signature cytokine IL-22 results in severely impaired maintenance of intestinal stem cells.

Decreased interleukin-27 signaling in humans and mice induces the formation of ectopic lymphoid-like structures (ELSs), which are associated with severe disease pathology and resistance to biological therapy in rheumatoid arthritis patients. Increased numbers of podoplanin-expressing Th17 cells in the absence of IL-27R signaling may be involved in driving ELS formation.

Immune cells of myeloid lineage cluster around amyloid-β plaques in the Alzheimer’s disease brain. However, assigning functional roles to myeloid subtypes, namely brain-resident microglia versus peripherally derived monocytes, has been problematic. Now, Varvel et al. use a model of central nervous system myeloid cell depletion to demonstrate that repopulation by peripheral monocytes is insufficient to eliminate plaques. The findings indicate that myeloid replacement therapy by itself may not be an effective therapeutic strategy in Alzheimer’s disease.

Prokop et al. demonstrate that conditional ablation of resident microglia in a mouse model of Alzheimer’s disease (AD) results in no significant change in amyloid-β burden, despite nearly complete replacement with peripheral myeloid cells. The findings suggest that additional triggers appear to be required to exploit the full potential of myeloid cell–based therapies for AD.

Viny et al. show that depletion of the cohesin subunit Smc3 affects HSC function through disruption of chromatin structure and that cohesin haploinsufficiency cooperates with Flt3-ITD to induce transformation of stem/progenitor cells and leukemia development.


Mullenders et al. report that loss of cohesin alters stem cell homeostasis and myelopoiesis, facilitating the development of a myeloid malignancy.

Vijay et al. show that an age-dependent increase of phospholipase A2 group IID (PLA2G2D) in the lung contributes to worse outcomes in mice infected with SARS-CoV. Mice lacking (PLA2G2D) had increased survival to lethal infection with enhanced DC migration to the dLN and augmented T cell responses. The results suggest that targeting (PLA2G2D) in elderly patients with respiratory infections could represent an attractive therapeutic strategy.

Song et al. generate mice selectively lacking NKp46+ ILC3s to demonstrate that in the absence of T cells, NKp46+ILC3s are sufficient to promote inflammatory monocyte accumulation in CD40-induced colitis via production of GM-CSF. In T cell–sufficient mice, the lack of NKp46+ILC3s did not impact C. rodentium infection.

Weber et al. identify TRPC6 as the calcium channel mediating the transient increase in endothelial cytosolic free calcium concentration required for transendothelial migration of leukocytes during the inflammatory response.

Yamamoto et al. report that PLA2G2F represents a previously unrecognized regulator of skin pathophysiology, and point to this enzyme as a novel drug target for epidermal-hyperplasic diseases.

Sawada et al. report that Resolvin E1 (RvE1) down-regulates DC motility in both steady state and inflammatory conditions in the skin and exerts its antiinflammatory effects in contact hypersensitivity. They propose the LTB4-BLT1 signaling blockade as a possible major mechanism through which RvE1 exerts its regulatory effects.

The mechanisms guiding cells toward bone surfaces are generally unknown. Here, Nevius et al. show that the Gαi protein–coupled receptor EBI2 is expressed in mouse osteoclast precursors to guide these cells toward bone surfaces. Defective EBI2 signaling increased bone mass in male mice and protected female mice from age- and estrogen deficiency–induced osteoporosis.

Hu et al. show that the chemokine receptor CCR4 is involved in thymocyte medullary entry, interactions with dendritic cells, and negative selection. In the absence of CCR4, central tolerance is not established, promoting autoimmunity.

Varney et al. report that that deletion of the TRAF-interacting protein TIFAB contributes to an MDS-like phenotype in mice by up-regulating TRAF6 and contributing to hematopoietic dysfunction.

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