During the COVID-19 pandemic, misinformation and vaccine hesitancy disproportionately affected ethnic minority communities across the United Kingdom, including in Wales. Muslim Doctors Cymru (MDC), a grassroots coalition of Muslim healthcare professionals, played a pivotal role in countering this challenge. This paper explores the strategies and impact of MDC’s work in addressing health misinformation, building trust, and promoting vaccine uptake among ethnic minority communities in Wales. Through culturally sensitive engagement, multilingual public health messaging, and close collaboration with mosques, community leaders, and local media, MDC delivered targeted outreach that bridged gaps between public health authorities and underserved populations. This case study draws on their grass-roots-efforts’ approach to tackling vaccine inequity using community-based approaches. Findings highlight the importance of culturally competent healthcare communication and the value of community-led initiatives in improving public health outcomes during crises. MDC’s model offers a replicable framework for addressing health inequalities and misinformation in diverse populations.

Natural killer (NK) cells are important lymphocytes of the innate immunological defense against cancer. Based on their molecular and functional phenotypes NK cells are categorized in two main subtypes known as CD56 dim and CD56 bright, with distinct transcriptomes profiles. Additionally, transcriptomic alterations may arise in response to different stimuli or milieu, ultimately affecting the NK cell behavior. Herein, RNA sequencing was carried out to characterize the transcriptomic profile of NK cells present in epithelial ovarian cancer (EOC)-associated ascites. Two bulk RNA sequencing datasets of isolated NK cells were analyzed; one generated from sampling of patients assisted at the Women’s Hospital of the University of Campinas (CAISM-Unicamp, Brazil) and the other made available at Gene Expression Omnibus database (GSE153713). Results identified 2829 differentially expressed genes (DEG ≥2 folds). RNA expression of genes encoding molecules associated with cytotoxic function ( NCR1, KLRK1, GZMB, PRF1) and maturation markers ( CLIC3, LAIR2, SPON2, CD160) were significantly downregulated in ascites NK cells. Alternatively, upregulated genes ( ICAM1, GZMK, IL18, IFNγ among others) strengthen to the ascites NK cells a transcriptomic profile consistent with the CD56 bright subtype. Finally, 120 upregulated genes were identified as highly correlated with the NCAM1/ FCGR3A expression ratio (ρ ≥0.7). Overall, these genes were interpreted as involved in suppression of signal transduction and intracellular signaling pathways, particularly redirecting the classical MAPK cascade to the p38MAPK. The transcriptomic profile of ascites NK cells included alterations consistent with lack of conventional blood cytotoxic cell characteristics, combined with an immature/secretory-like profile, assigned to the CD56 bright subtype of NK cells.

Dysregulated copper ion homeostasis is a key factor in disrupting the immune microenvironment of diabetic wounds. However, conventional copper delivery systems are limited by unstable release kinetics and transient therapeutic effects. To address these challenges, this study introduces a long-acting copper ion-releasing hydrogel (GelMA@HKUST-1) based on a metal-organic framework (HKUST-1), designed to promote diabetic wound healing by modulating neutrophil function. In vitro analysis demonstrated that copper ions released from the hydrogel significantly suppressed hyperglycemia-induced neutrophil extracellular trap (NETosis) formation, while restoring immune function through the promotion of neutrophil apoptosis. In antibacterial assays, although the hydrogel exhibited limited direct bactericidal activity, it effectively reduced bacterial burden and enhanced host immune defense by inhibiting NETosis and accelerating neutrophil apoptosis. Additionally, in vivo studies revealed that the porous structure of HKUST-1 enabled sustained copper ion release for over one week, significantly accelerating wound healing in diabetic mice without causing systemic toxicity. This study proposes a dual regulatory mechanism for copper-mediated immunomodulation—balancing NETosis inhibition and apoptosis activation to optimize antibacterial efficacy—providing a novel therapeutic strategy with prolonged action and improved safety for diabetic wound management.

Gastrointestinal symptoms have emerged as a common, but underappreciated, cause of morbidity in relation to SARS-CoV-2 infection and the COVID-19 pandemic. This manifests as a range of indications including diarrhea, anorexia, nausea, vomiting and abdominal pain. In addition, the gastrointestinal tract may represent a route of viral entry via the epithelial cell layer lining the gut wall. This route of entry could be a significant component of disease pathogenesis, including effects on the nervous system via the gut-brain axis. In this review we provide an assessment of the effects of COVID-19 on the gastrointestinal system, its involvement in disease severity and potential pathways for viral entry and infection in the gastrointestinal tract. We also examine evidence that gut-derived serotonin is affected by SARS-CoV-2 infection, how this may link to symptoms and disease pathogenesis, and the potential link to the efficacy of selective serotonin reuptake inhibitors in reducing COVID-19 severity.

BACKGROUND: Responses to immune perturbations can vary greatly when comparing geographical regions such Europe versus South East Asia but also when comparing urban versus rural areas within a country. This can translate into differences in disease profiles or in responses to vaccines. However, even within an urban area, large differences in income settings can be seen. Therefore, it is also important to assess whether differences observed when comparing rural and urban residents can also be detected between high and low socioeconomic status (SES) within an urban center. AIM: To examine the immune profile of children of high versus low SES METHODS: Using mass cytometry, we profiled immune cells in finger-prick blood samples of children attending high and low SES schools in Makassar, Indonesia. RESULTS: Significant differences were found in the immune profiles of children from low versus high SES. Increased frequencies of entire and CD11c+ B cells, CD161+ T helper 2 cells and CTLA-4+ Tregs and HLA-DRdimCD163+ monocytes were seen in low SES children, whereas a trend towards expansion of T helper 1 cells was observed in the high SES group. CONCLUSION: Although differences in the immune system of populations living in rural versus urban areas have been documented, this study shows that within an urban center, the socioeconomic status can have a significant impact on the immune system of children. Such differences might contribute to variation seen in immune reactivity to allergens, autoantigens or vaccines, therefore SES should be factored in when studying responses to immune perturbations.

The Gastroenterology Immunology Neuroscience (GIN) Discovery Program represents a new model for research that overcomes the limitations imposed by traditional ‘research silos’ in medical science. By adopting a cross-disciplinary, highly-integrated approach, the GIN Program unites the fields of gastroenterology, immunology, and neuroscience to comprehensively address chronic health challenges. This initiative not only bridges the gaps between basic science, clinical research, and patient care but also emphasises the importance of diversity in ideas, perspectives, and approaches when fostering innovation. The program’s organic, bottom-up growth strategy has facilitated the formation of a vibrant, interdisciplinary community, captivating attention from both national and international institutions. With a vision to create effective therapeutic solutions and pioneer advancements in gut-immune-brain axis research, the GIN Program exemplifies the power of interdisciplinary collaboration. This innovative commitment to change the landscape of medical research aims to inspire similar models that prioritise open communication, mutual respect, and a commitment to groundbreaking science.

CD8+ T cells recognising their cognate antigen are typically recruited as a polyclonal population consisting of multiple clonotypes with varying T-cell receptor (TCR) affinity to the target peptide-MHC (pMHC) complex. Advances in single-cell sequencing have increased accessibility towards identifying TCRs with matched antigens. Here we present the discovery of a monoclonal CD8+ T cell population with specificity for a hepatitis C virus (HCV)-derived HLA class I epitope (HLA-B*07:02 GPRLGVRAT) which was isolated directly ex vivo from an individual with an episode of acutely resolved HCV infection. This population was absent prior to infection and underwent expansion and stable maintenance for at least two years after infection as measured by HLA-multimer staining. Furthermore, the monoclonal clonotype was characterised by an unusually long dissociation time (half-life = 794 seconds and koff = 5.73×10-4) for its target antigen when compared to previously published results. A comparison with related populations of HCV-specific populations derived from the same individual and a second individual suggest that high-affinity TCR-pMHC interactions may be inherent to epitope identity and shape the phenotype of responses which has implications for rational TCR selection and design in the age of personalised immunotherapies.

Individuals with low socioeconomic status (SES) are at greater risk of contracting and developing severe disease compared to people with higher SES. Age, sex, host genetics, smoking, and Cytomegalovirus (CMV) serostatus are known to have a major impact on human immune responses and thus susceptibility to infection. However, the impact of SES on immune variability is not well understood or explored. Here, we used data from the Milieu Intérieur project, a study of 1,000 healthy volunteers with extensive demographic and biological data, to examine the effect of SES on immune variability. We developed an Elo-rating system using socioeconomic features such as education, income, and household to objectively rank SES in the 1,000 donors. We observed sex specific SES associations, such as females with a low SES having significantly higher frequency of CMV seropositivity compared to high SES females, and males from a low SES having significantly higher frequency of active smoking compared to high SES males. Using random forest models, we identified specific immune genes which were significantly associated with SES in both baseline and immune challenge conditions. Interestingly, many of the SES associations were sex-stimuli specific, highlighting the complexity of these interactions. Our study provides a new way of computing SES in human populations that can help identify novel SES associations and reinforces biological evidence for SES-dependent susceptibility to infection. This should serve as a basis for further understanding the molecular mechanisms behind socioeconomic status effects on immune responses and ultimately disease.

This journey traces the transition from a brief dentistry stint to a neuroimmunology exploration. The narrative unfolds through academic pursuits at the University of São Paulo, Brazil, and subsequent doctoral studies, reflecting on the initial idealism that shaped the pursuit of academia. An unexpected postdoctoral experience at the Centre de Physiopathologie de Toulouse Purpan in France introduced me to immunology, leading to an unexpected passion. Here, I explore uncertainties, decisions, and a pivotal move to Belgium, where collaboration with Adrian Liston at VIB-KU Leuven marked a maturity phase. Amid personal milestones like pregnancy and the challenges of balancing parenthood with a burgeoning career, I would like to highlight the crucial role of support systems and a thriving research environment. My journey so far culminates in the establishment of a lab, the pursuit of a permanent position, and the appointment as an assistant professor at KU Leuven.

Effective vaccines have reduced SARS-CoV-2 morbidity and mortality; however, the elderly remain the most at risk. Understanding how vaccines generate protective immunity, and how these mechanisms change with age is key for informing future vaccine design. Cytotoxic CD8+ T cells are important for killing virally infected cells, and vaccines that induce antigen specific CD8+ T cells in addition to humoral immunity provide an extra layer of immune protection. This is particularly important in cases where antibody titres are sub-optimal, as can occur in older individuals. Here, we show that in aged mice, spike-epitope specific CD8+ T cells are generated in comparable numbers to younger animals after ChAdOx1 nCoV-19 vaccination, although phenotypic differences exist. This demonstrates that ChAdOx1 nCoV-19 elicits a good CD8+ T cell response in older bodies, but that typical age-associated features are evident on these vaccine reactive T cells.