Millennium Institute on Immunology and Immunotherapy

The electrochemical reduction of CO2 (ECO2RR) has emerged as a promising route for converting CO2 into value‐added chemicals and fuels using renewable electricity. Among transition metals, copper uniquely enables the formation of C1 and C2 products, but it suffers from poor selectivity and stability in its monometallic form. This review explores recent advances in Cu–Zn and Cu–Bi bimetallic systems, emphasizing how their structural, electronic, and interfacial characteristics influence ECO2RR pathways and product distribution. Mechanistic insights into active site behavior, alloying effects, and the role of surface facets are provided. Limitations such as catalyst degradation and scalability are critically discussed, including a comparing performance across different electrochemical cell configurations. Finally, design guidelines and future research directions are proposed to enhance Cu‐based bimetallic catalysts’ selectivity, stability, and scalability for ECO2RR.

Zika virus (ZIKV) is a mosquito-borne flavivirus causing a major epidemic in the Americas in 2015. Dendritic cells (DCs) are leukocytes with key antiviral functions, but their role in ZIKV infection remains under investigation. While most studies have focused on the monocyte-derived subtype of DCs, less is known about conventional dendritic cells (cDCs), essential for the orchestration of antiviral adaptive immunity. This study investigates the mechanisms by which cDCs respond to ZIKV for antiviral cytokine production. Here, using murine cultures, we demonstrate that ZIKV infection and not detection of ZIKV-infected dead cells activates cDCs by inducing type I interferons (IFN-I) and proinflammatory cytokines. Furthermore, ZIKV-infected cDCs markedly activated the IRE1/XBP1s axis of the unfolded protein response (UPR). Flow cytometry analysis indicates that among cDCs, type 1 cDCs (cDC1s) are responsible for ZIKV detection. Functionally, genetic loss of XBP1s curtailed expression of the costimulatory molecule CD86 and the production of IFN-I and proinflammatory cytokines by cDCs, without exhibiting increased susceptibility to ZIKV infection. These effects are attributable to perturbations in the IRE1/XBP1s axis and not due to overcompensation of PERK or IRE1 kinase signaling. Finally, tissue resident cDCs also exhibit susceptibility to infection, potentially establishing these cells as ZIKV targets invivo. These findings underscore a critical role for the IRE1/XBP1s pathway in fine-tuning cDC activation to ZIKV, linking viral recognition to cDC functional maturation and opening new avenues for exploring UPR pathways targeting cDCs in the context of flavivirus infections.

Phylogeographic studies in Antarctica allow us to understand the demographic events of populations during glacial periods. In this study, the polyplacophoran Tonicina zschaui was analyzed in several localities on the West Antarctic Coast using the mitochondrial gene cytochrome oxidase subunit I (COI). Two genetically distinct populations were identified: one in the Weddell Sea and another across the Antarctic Peninsula and South Shetland Islands. Genetic diversity was generally low to moderate, suggesting limited gene flow and the influence of historical climatic events. Star-like haplotype networks and demographic analyses indicate population contractions during the Last Glaciation followed by postglacial expansion, especially in the Antarctic Peninsula–South Shetland Islands population. Several sites in this region were identified as potential glacial refugia, exhibiting proportionally elevated genetic diversity and exclusive haplotypes. Conversely, the small Weddell Sea population displayed signs of long-term isolation, limited expansion, and low diversity, likely due to stronger environmental constraints and genetic drift. Ocean currents such as the Antarctic Coastal Current, the Antarctic Peninsula Coastal Current and the Weddell Gyre appear to restrict larval dispersal, reinforcing genetic discontinuities. These findings support the hypothesis of glacial survival in localized refugia and postglacial recolonization, a pattern observed in other Antarctic marine invertebrates.

Infectious; IRCCS Ospedale San Raffaele, Milan, Italy.Barrier tissues separate the external environment from the internal environment of the human body. These specialized structures serve not only as passive physical barriers but also as dynamic regulators of molecular and cellular traffic, thereby playing a critical role in maintaining physiological homeostasis. Barrier integrity is essential across multiple systems, including the respiratory, urinary, gastrointestinal, and sensory systems. In pathological states, disruption of barrier function permits the translocation of inappropriate or excessive molecular species, which can precipitate aberrant immune activation, often skewed toward pro-inflammatory responses. Such immune dysregulation may exacerbate existing pathology or contribute to the onset of comorbid conditions.This research topic sheds light on the pathophysiology of barrier tissues is disease contexts across multiple organ systems. It emphasizes the underlying mechanisms of barrier tissue dysfunction and the immune system's role in these processes, while highlighting potential biological models and outlining future clinical research directions to manage diseases with barrier tissues in mind.The mini review by Simalee et al. describes the pathogenic roles and effects of inflammatory eosinophils (iEOS) and tissue resident eosinophils (rEOS) in Chronic rhinosinusitis with nasal polyps (CRSwNP). Simalee et al. discussed different populations of eosinophils and how an imbalance of iEOS and rEOS exacerbates the type 2 endotype of CRSwNP, both due to eosinophil mechanisms and by signaling to other immune cells. The authors also placed a heavy focus on the potential impact of CRSwNP treatments which further exploration of eosinophil population may offer; this includes anti-eosinophilia drug treatment or combinations and using subtypes of eosinophils as biomarkers in clinical disease management and as predictor variables in models.In their perspective article, Jin et al. explore the role of circulating immune complexes in the development of arthritis among patients with inflammatory bowel disease (IBD).They highlight how increased intestinal permeability, or "leaky gut", in IBD allows microbial products to enter the circulation. This translocation facilitates the formation and systemic distribution of immune complexes, which may deposit in joints and trigger inflammatory responses. The authors further discuss potential strategies to restore gut barrier integrity, emphasizing the therapeutic potential of butyrate, a short-chain fatty acid known to support epithelial health and reduce permeability. This work underscores the gut-joint axis as a possible target for preventing extraintestinal complications of IBD.The PrEP-treated and control groups, suggesting that oral PrEP does not compromise the mucosal epithelial barrier. Additionally, while TJ genes correlated with cytokine signaling, PrEP had no significant impact on inflammatory gene expression. These findings support the safety of oral PrEP in preserving epithelial integrity and encourage further investigation into its broader biological effects.In conclusion, this research topic highlights recent advancements in the study of barrier tissues across multiple organ systems. This topic presents clinically relevant discussions and insights into how dysfunctional barrier tissues may participate with health disorders. This topic aims to encourage further studies on barrier tissues and translational research, showcasing innovative models for studying barrier function, progress in biomarker discovery, and the development of novel diagnostic and treatment strategies.