Volume 16 Issue 8, August 2015

Effective anti-tumor immune therapy in solid tumors relies on the presence of effector T cells. Inhibition of the dipeptidylpeptidase DPP4 (CD26) enhances chemokine CXCL10–mediated infiltration of lymphocytes into the tumor parenchyma, which results in diminished tumor growth.

Targeted deletion of the transcription factor XBP1 in hematopoietic stem cells selectively prevents eosinophil maturation in the bone marrow without affecting other lineages of the immune system.

As the cytosolic guardian for many microbial and sterile inflammatory insults, NLRP3 is best appreciated for its innate immunological role mediating inflammasome activation. Now NLRP3 debuts as a transcription factor key for T_H2 polarization.

Fat-associated lymphoid clusters (FALCs) are non-classical secondary lymphoid organs of the body cavities. The formation and maturation of FALCs are driven by tumor-necrosis factor and are further enhanced by invariant natural killer T cells.

Type I and III interferons share similar antiviral properties, but there are some important distinctions. Hartmann and colleagues review the specialized functions of type III interferons, including their ability to mediate antiviral functions at barrier surfaces.

Hematopoietic stem cells are held in check to maintain their functional activity throughout life. Qian and colleagues show that the transcriptional regulator Foxm1 maintains the quiescence and self-renewal capacity of these cells in vivo.

Fat-associated lymphoid clusters are lymphoid tissues that support B-1 cells. Caamaño and colleagues show that inflammation that elicits the cytokine TNF and activates natural killer cells contributes to the formation of these clusters in visceral fat.

The transcription factor XBP1 is associated with endoplasmic reticulum stress. Glimcher and colleagues show that XBP1 is expressed during eosinophil differentiation and is uniquely required for the production of granule proteins and eosinophil survival.

Interferon-γ (IFN-γ) primes macrophages to undergo proinflammatory activation. Ivashkiv and colleagues detail the translational and metabolic program triggered in human macrophages after IFN-γ treatment.

Post-translational modification of chemokines such as CXCL10 can regulate their activity. Albert and colleagues demonstrate that the endogenous peptidase DPP4 cleaves CXCL10 and thereby interferes with T cell recruitment to tumors.

The receptor NLRP3 is central to the formation of inflammasomes in myeloid cells. Ghiringhelli and colleagues demonstrate that NLRP3 also serves an important inflammasome-independent role in CD4⁺ T cells, in which it helps coordinate T_H2 differentiation.

The precise factors that control effective memory formation by T cells are unclear. Kaech et al. demonstrate that regulatory T cell–produced IL-10 is critical for the generation of CD8⁺ memory cells.

Secretory IgA (SIgA) shapes the gut microbial composition. Pabst and colleagues show that the IgA-secreting plasma cell repertoire, once established, is remarkably resilient to changes in microbial populations that occur upon infection or antibiotic treatment.