Bioelectric signaling as an emerging layer of macrophage communication #immunology
A pancreatic intraepithelial neoplasia—Oramic view of early pancreatic cancer in 3D #immunology
Promoting intestinal regeneration without tumor risk in immune-mediated inflammatory diseases #immunology
TGF-β: A master regulator of tissue-resident macrophage identity and function #immunology
Parental leave in immunology — 5 #immunology
SIRT6 bridges glycolysis and epigenetics to neutrophilic asthma #immunology
DNA sensing and regulation of lipid metabolism #immunology
Trends in Immunology
Trends in Immunology
Trends in Immunology
Trends in Immunology
Trends in Immunology
Trends in Immunology
Trends in Immunology
Trends in Immunology
Group 3 innate lymphoid cells: guardians of intestinal homeostasis.
Jiacheng Hao,Xiaohuan Guo
“Intestinal homeostasis is crucial for overall health, and its maintenance relies on a complex and delicate interplay between intestinal epithelial cells, the gut microbiota, and the immune system.”
Pancreatic cancer is a deadly disease defined by an immunosuppressive microenvironment refractory to therapy. Kiemen et al. applied 3D histology, imaging mass cytometry, and spatially resolved DNA sequencing to human pancreata containing early precursors of the disease, revealing heterogeneous and mutation-specific inflammatory niches that are poorly resolved by 2D methods.
I am a cancer immunologist and a junior group leader in precision immuno-oncology in Milan, Italy. My work focuses on developing personalized immunotherapy strategies for solid tumors, generating patient-specific tumor-reactive T cells, and investigating how tumors escape immune surveillance. In November 2022, while I was a postdoctoral researcher in Italy, I took parental leave following the birth of my child.
Neutrophil asthma is a severe, corticosteroid-resistant subtype characterized by airway neutrophilia and declining lung function. Su et al. identify a sirtuin 6–lactate dehydrogenase A–histone lactylation axis that links macrophage glycolysis to epigenetic chemokine regulation, offering mechanistic insight into neutrophil recruitment and highlighting potential therapeutic targets.
I am an immunologist with over 15 years of experience in translational biomedical research, specializing in T cell biology, autoimmune diseases, and gastrointestinal cancers. My work explores how immune cells maintain balance, drive inflammation, and regulate epithelial transformation, with a growing focus on immune–microbiome interactions and strategies to therapeutically modulate them. I also earned an Executive MBA to support this translational vision. Beyond research, I am committed to advancing women’s participation in science, promoting gender-responsive medicine in inflammatory bowel disease and colon cancer, and fostering connections between patient associations and key stakeholders.
Immune-mediated inflammatory disorders, such as inflammatory bowel diseases, are characterized by chronic inflammation and damage to the intestinal barrier. Several of the current therapeutic strategies for inflammatory diseases attempt to decrease inflammation but cause side effects in a significant fraction of patients without promoting remission. Leveraging the power of intestinal regeneration for therapeutic purposes holds great promise, but it comes with the significant risk of promoting tumorigenesis, as most of the pathways that boost the regenerative program are also exploited by tumor cells for their growth and survival. In this article, we review the common mechanisms promoting intestinal regeneration and tumor development and discuss the latest studies identifying cellular and molecular pathways that promote regeneration but not tumorigenesis.
Bioelectric signaling may represent an emerging layer of macrophage communication. This forum discusses how membrane-potential dynamics, ion fluxes, and context-dependent intercellular coupling may coordinate macrophage responses within tissues, highlighting a potential new dimension of immune regulation with broad implications for tissue-level immunity.
Tissue-resident macrophages exhibit remarkable plasticity, dynamically adapting to their local environment and adopting tissue-specific phenotypes that support organ homeostasis. The underlying identity-determining transcriptional programs are instructed by microenvironmental cues. Transforming growth factor-β (TGF-β), which has long been recognized for its role in immunosuppression, has recently emerged as a pivotal determinant of tissue macrophage identity. In this review, we highlight how TGF-β shapes innate immunity by driving macrophage imprinting and transcriptional programming within defined tissue niches. We emphasize that the spatial and temporal regulation of TGF-β activation—rather than its overall abundance—governs its divergent effects on immune cells. Understanding the precise mechanisms promises to spur the development of more selective therapeutic strategies for modulating macrophage function in health and disease.
dlvr.it
Immunity and metabolism are deeply intertwined in maintaining homeostasis. With the recognition of cytosolic dsDNA sensing as an initiator of immune responses, its interface with metabolic rewiring has emerged as a key area of investigation. Focusing on the stimulator of interferon genes adaptor protein, critical for dsDNA-mediated inflammation, we examine the link between lipid metabolism and innate immunity. Adopting an evolutionary perspective and through comparisons with the inflammasome pathway, also specialized in innate immune activation, we explore the conservation of this interface across innate immune systems. We propose that the connection between dsDNA sensing and metabolism could unlock innovative precision medicine strategies for inflammatory diseases.