Volume 18 Issue 8, August 2017

Netea and colleagues provide a general guide to the cellular and humoral contributors to inflammation as well as the pathways that characterize inflammation in specific organs and tissues.

Kastner and colleagues review monogenic autoinflammatory diseases and their molecular mechanisms and explore the overlap among autoinflammation, autoimmunity and immunodeficiency.

Kroemer and colleagues discuss the mechanisms through which nutrition modulates metabolic, microbial and neuroendocrine circuitries that affect cancer development and the response to treatment.

Magarian Blander and colleagues review the effects of the microbiome on innate and adaptive immunological players and how microbiota-derived bioactive molecules affect inflammation and the host response to infection, vaccination and cancer.

Beyaert, Karin and colleagues discuss the key molecular mechanisms that contribute to the self-limiting nature of inflammatory signaling, with emphasis on the negative regulation of the NF-κB pathway and the NLRP3 inflammasome.

The infiltration of solid tumors by CD8⁺ T cells is a favorable prognostic marker. Large-scale transcriptome analysis of tumor-infiltrating T cells from mucosal tumors shows that CD8⁺ T cells with a CD103⁺ tissue-resident memory T cell phenotype might be the most desirable.

Lineage bias among early hematopoietic progenitor cells is specified by transcription-factor programming, and lineage switching reduces the quantity of cells produced.

Uncoupling of activation of Fc receptors via a mutant IgG1 Fc domain shows a direct role for complement receptors in antibody-dependent tumor killing.

Liu and colleagues show that specification of the dendritic-cell lineage occurs in parallel with specification of the myeloid and lymphoid lineages in or around the hematopoietic-stem-cell stage, starting as a lineage bias defined by transcriptional programs that correlate with the combinatorial dose of IRF8 and PU.1.

Monoclonal antibody (mAb) therapy is now commonplace in the clinic, yet such reagents can elicit unwanted side effects due to interactions with Fcγ receptors. Georgiou and colleagues have engineered mAbs that lack such FcγR interactions but retain the ability to activate complement and show that these modified mAbs have efficacious effector function.

Various intracellular pathogens attempt to hide from innate cytosolic sensors by forming vacuoles. Yamamoto and colleagues show that the autophagy-related protein Gate-16, which is induced by interferon-γ, is required for noncanonical autophagy to control infection by Toxoplasma gondii.

Expression of a competent Igh heavy chain initiates a pre-BCR checkpoint during B cell development. Reth and colleagues show that protein arginine methylation by a BTG2-PRMT1 complex is required to inactivate CDK4 and thereby establish pre-B cell arrest.

Germinal centers generate high-affinity memory B cells. Qi and colleagues identify a precursor of memory B cells in germinal centers and demonstrate that the cytokine IL-9-derived from follicular helper T cells is important for their development into full-fledged memory cells.

Xue and colleagues show that Runx3^−/− CD8⁺ T effector cells aberrantly upregulate genes characteristic of T_FH cell lineage and exhibit impaired induction of cytotoxic molecules.

Vijayanand and colleagues use genome-wide RNA sequencing for transcriptional profiling of CD8⁺ T cells from tumors and adjacent uninvolved lung tissue from patients with early-stage lung cancer. A tissue-resident memory signature is associated with enhanced cytotoxicity and improved survival.