Volume 14 Issue 6, June 2013

The mast cell–derived phospholipase PLA2G3 and fibroblast prostaglandin synthase contribute to a mast cell–fibroblast paracrine axis dependent on the prostaglandin PGD₂ and its receptor DP1 that can enhance the maturation and mediator secretion of mast cells.

An algorithm developed with a systems-biology approach reconstructs some of the key regulatory events known to drive the development of cells of the mouse immune system and makes many other novel predictions for testing.

Repeated antigenic and inflammatory stimulation during chronic infection is thought to produce 'exhausted' T cells. However, persistent viruses also generate PD-1^hi CD8⁺ T cells with proliferative and cytotoxic ability but 'censored' inflammatory function.

Either stimulation of the innate immune system or infection can result in transient focal inflammatory structures in the liver. Such structures can promote further proliferation of already activated cytotoxic T lymphocytes and enhance antipathogen immunity.

The NLRP3 inflammasome is primarily known for producing inflammatory cytokines and inducing pyroptosis. Stuart and colleagues identify an additional role for NLRP3 in driving down the pH of phagosomes.

The mechanisms controlling maturation of mast cells toward an anaphylaxis-sensitive phenotype remain unclear. Murakami and colleagues show that PLA2G3, a mammalian homolog of anaphylactic bee venom phospholipase A₂, regulates this process.

Innate lymphoid cells (ILCs) have been found in gut and lungs. Weninger and colleagues identify IL-13-producing ILCs in the skin, where they interact with mast cells and regulate allergic responses.

Chronic infections are commonly established in the liver. Knolle and colleagues show that cytotoxic T lymphocyte responses can be boosted by TLR-mediated induction of myeloid aggregates (iMATES).

The developmental requirements of IL-17-committed γδ T cells remain unclear. Cyster and colleagues show that the transcription factor Sox13 is selectively required for the development of the Vγ4⁺ subset of γδ T cells.

The roles of individual microRNAs in the CD8⁺ T cell response remain mostly unexplored. Katsikis and colleagues show that miR-155 regulates type I interferon responsiveness and CD8⁺ T cell responses to pathogens in vivo.

During chronic infection, pathogen-specific CD8⁺ T cells are thought to terminally differentiate into exhausted cells. However, Zehn and colleagues show that T cells with memory-like properties are generated during such infections.

The Akt-mTOR axis influences cell activation, differentiation and metabolism. Jordan and colleagues show that thymic and inducible T_H17 cells exhibit different requirements for mTORC1 and mTORC2 as well as Akt isoforms.

The differentiation of αβ T cells is a complex process. Using data sets from the Immunological Genome Project, Benoist and colleagues identify candidate mediators of key transitions during thymocyte selection and maturation.

The transcriptional circuitry that controls the differentiation of hematopoietic stem cells into cells of the immune system is only partially understood. Koller and colleagues use a computational algorithm to identify previously unknown differentiation stage–specific regulators of mouse hematopoiesis.