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In this issue, we are proud to feature a collection of articles on inflammatory disease (pp 669740). The cover image depicts the epithelium that lines the mouse gastrointestinal tract and influences immunity. The cell membrane of small intestinal epithelial cells is visualized in green with the nuclei shown in orange. Paneth cell granules at the base of the crypts are marked in blue. Image courtesy of Mario Noti, Gregory F. Sonnenberg and David Artis. Artwork by Erin Dewalt.
Two new studies demonstrate that so-called 'liquid biopsies' may reveal important genomic information needed to monitor treatment responses, forecast tumor recurrences, and provide a rationale for novel therapeutic strategies in patients with lung cancer and colon cancer.
Muscle fibrosis after acute injury can be debilitating, but in chronic muscle disease it can be lethal. A new study reveals that shifts in macrophage phenotype in injured or diseased muscle can influence whether connective tissue production by fibro/adipogenic precursors in muscle is beneficial or pathological.
Adipocyte progenitors have the capacity to differentiate into mature brown adipocytes with thermogenic capabilities. Two new studies identify novel markers to help prospectively isolate these and mature adipocytes from human brown fat biopsies.
Inflammatory disease research is burgeoning. Large data sets are being generated to characterize the human immune response, while detailed mechanistic studies are defining the role of specific cell types and sensors in inflammatory disease. Future efforts are needed to integrate these approaches and guide precision medicine.
As it becomes evident that the microbiome exerts an influence on the human immune system, scientists have begun to ponder therapies that might act on intestinal microbes to reduce harmful inflammation. Roxanne Khamsi reports.
Tissue-resident memory T cells are increasingly being linked to human tissue-specific immune and inflammatory disease. These roles are discussed in this review.
Recent studies have provided insight into how the environment, and in particular the diet, influence the development of lymphocytes. Emerging studies indicate a role for this immune development in inflammatory disease.
Cua and colleagues discuss the cellular and molecular rationale for targeting IL-12 and IL-23 for therapeutic purposes in inflammatory diseases; they also review existing clinical data, discuss potential side effects, and propose future directions for targeting these cytokines in additional disorders.
Recent advances in genetics have deepened our understanding of the pathogenic mechanisms behind autoimmune and immune-mediated diseases. This has revealed both shared pathways and a considerable degree of heterogeneity between diseases.
Epigenetic inactivation of a Rab GTPase activating protein confers metastatic properties in melanoma, and it correlates with poor prognosis but better sensitivity to therapy by targeting EGFR signaling.
Whole-genome and targeted sequencing of multiple sections of each of 50 tumors reveals varying degrees of subclonal diversification and genomic heterogeneity.
Human brown and white preadipocyte clones from neck fat depots have been isolated and used to identify genetic biomarkers that predict their thermogenic capacity.
Ucn3 is released from pancreatic beta cells along with insulin, and it engages a negative feedback loop by promoting somatostatin secretion from delta cells to control further insulin secretion.
BMP9 activates signaling through the BMPR-II receptor in endothelial cells and reverses established disease in three animal models of pulmonary hypertension, thus pointing to a potential new treatment for this disease.
Tgf-β1 contributes to fibrosis during chronic injury by abrogating Tnf-directed apoptosis of fibro/adipogenic progenitor cells during muscle regeneration
By monitoring ctDNA, the authors reveal the dynamic adaption of clonal populations in colorectal cancer patients treated with anti-EGFR therapy, suggesting that therapeutic re-challenge may have some benefit.
The introduction of α-synuclein into mouse models of Alzheimer's disease, either by intracerebral injection or transgenic overexpression, is found to inhibit the formation of hippocampal amyloid-β plaques.
There is an emerging understanding of how the disruption of immune homeostasis may lead to the development of chronic inflammatory diseases. This series of articles highlights new data that point toward the influence of environmental factors and addresses recent advances in our knowledge of the cell types and signaling pathways involved in inflammatory disease onset and progression.