We are pleased to highlight a selection of impactful articles published in the BSI’s official journals, Immunotherapy Advances, Discovery Immunology and Clinical & Experimental Immunology over the past year. These standout papers were selected due to their high number of article downloads, citations or wider reach, and span topics from immune regulation and infection biology to autoimmunity and cancer immunotherapy, reflecting the research that has captured the attention of our global community.
Discovery Immunology
DOI: 10.1093/discim/kyaf002
Henriette Arnesen, Signe Birkeland, Harriet Stendahl, Klaus Neuhaus, David Masopust, Preben Boysen, Harald Carlsen
Researchers compared multiple “naturalization” methods in mice and found that different microbial exposures, especially co‑housing with wild mice, produce distinct effects on gut microbiota, epithelial gene expression, and immune cell composition. These insights help guide the selection of naturalized mouse models for studies aiming to better reflect real‑world immune and gut barrier responses.
Obesity drives dysregulation in DC responses to viral infection
DOI: 10.1093/discim/kyaf001
Andrea Woodcock, Ronan Bergin, Nidhi Kedia-Mehta, Cathriona Foley, John C Stephens, Donal O’Shea, Mary Canavan, Andrew E Hogan
This study shows that dendritic cells from mice with diet‑induced obesity produce fewer cytokines when faced with a viral infection, linked to impaired cellular metabolism and reduced protein translation. These obesity‑driven defects may weaken downstream immune responses, increasing vulnerability to viral illness.
Dynamic roles of ILC3 in endometrial repair and regeneration
DOI: 10.1093/discim/kyaf004
Antonia O Cuff, Ee Von Woon, Thomas Bainton, Brendan Browne, Phoebe M Kirkwood, Frances Collins, Douglas A Gibson, Philippa T K Saunders, Andrew W Horne, Mark R Johnson, David A MacIntyre, Victoria Male
ILC3 cells in the uterus shift between two subsets that become active at different stages of the menstrual cycle and after birth, helping drive tissue repair and regeneration. In endometriosis, these cells sit farther from the tissues they normally support, which may impair healthy endometrial healing.
DOI: 10.1093/discim/kyae017
Yolanda Corripio-Miyar, Adam D Hayward, Hannah Lemon, Xavier Bal, Cameron Cunnea, Fiona Kenyon, Jill G Pilkington, Josephine M Pemberton, Daniel H Nussey, Tom N McNeilly
T‑helper immune responses in wild Soay sheep are surprisingly flexible: instead of opposing each other, Th1 and Th2 signals often rise together and consistently reflect resistance to different parasites. Though antibody levels are stable over time, T‑helper cell counts vary widely between individuals, highlighting how complex and dynamic immune strategies are in natural environments.
CD28 and TCR differentially impact naïve and memory T cell responses
DOI: 10.1093/discim/kyaf006
Cayman Williams, Dalisay Giovacchini, Alan Kennedy, Neil Halliday, Erin Waters, Maximillian Robinson, Claudia Hinze, David M Sansom
CD28 signalling doesn’t just amplify T‑cell activation, it shapes naïve and memory T cells in distinct ways. This study shows that the balance between CD28 and TCR signals determines how these cells divide and function, with memory T cells even showing CD28‑driven effects independent of the TCR, revealing a far more complex interplay than previously appreciated.
Clinical & Experimental Immunology
Sabine Weber, Xinyi Wei, Guixia Chen, Katharina Yankouskaya, Decheng Yin, Ida Allabauer, Tilman Jobst-Schwan, Michael Wiesener, Mario Schiffer, Diana Dudziak, Christian H K Lehmann, Joachim Woelfle, André Hoerning
mTOR‑inhibitor therapy after kidney transplant suppresses key signalling (p70S6K phosphorylation) in specific dendritic cell and NK‑cell subsets, but not uniformly across all immune cells. Measuring this signalling directly, rather than relying on drug blood levels may offer a more accurate, personalised way to gauge immunosuppressive effectiveness.
FcγRIIB (CD32B) antibodies enhance immune responses through activating FcγRs
DOI: 10.1093/cei/uxaf015
Alexander P Simpson, Robert J Oldham, Kerry L Cox, Martin C Taylor, Sonya James, Ann L White, Yury Bogdanov, Martin J Glennie, Björn Frendeus, Mark S Cragg, Ali Roghanian
Blocking the inhibitory receptor FcγRIIB with antibodies boosts antibody production and improves tumour clearance, not by removing inhibitory signals but by promoting Fc‑mediated activation of other Fcγ receptors. The study suggests that FcγRIIB‑targeting antibodies could be a powerful new strategy to enhance vaccine effectiveness.
Neuro-Behçet’s disease: an update of clinical diagnosis, biomarkers, and immunopathogenesis
DOI: 10.1093/cei/uxae123
Haoting Zhan, Linlin Cheng, Yongzhe Li
Neuro‑Behçet’s disease is a rare but severe neurological manifestation of Behçet’s disease, diagnosed mainly through clinical features and MRI because reliable lab biomarkers are still lacking. Emerging evidence highlights IL‑6 and other inflammatory markers as key indicators of disease activity, while immune imbalance and autoantibodies reveal the autoimmune and inflammatory mechanisms driving CNS damage.
Human genetics of responses to vaccines
DOI: 10.1093/cei/uxaf034
Eleanor Karp-Tatham, Julian C Knight, Alexandre Bolze
Genetic differences help explain why people vary so much in how strongly they respond to vaccines, and why rare adverse reactions occur in only a small subset of individuals. Large‑scale studies, especially during COVID‑19, have revealed clear links between specific HLA variants and vaccine responses, opening the door to safer, more effective, and more personalised vaccination strategies.
DOI: 10.1093/cei/uxae115
Katie J Smith, Zachary Lim, Sonja Vermeren, Veronique E Miron, Sarah Dimeloe, Donald J Davidson, Anna Williams, Emily Gwyer Findlay
Neutrophils from people with Multiple Sclerosis show major protein‑level differences compared to healthy individuals, including an overabundance of inflammatory granule proteins and altered MAVS‑pathway signalling. These dysregulated neutrophils also fail to properly suppress T‑cell activation, especially pathways linked to Th17 cells suggesting they may contribute directly to the immune imbalance that drives MS.
Immunotherapy Advances
Bispecific T-cell engagers for the recruitment of T cells in solid tumors: a literature review
DOI: 10.1093/immadv/ltae005
Laura Dewaele, Ricardo A Fernandes
BiTEs can successfully redirect T cells to kill cancer cells without relying on normal MHC–TCR interactions, but they’ve struggled to work in solid tumors because of toxicity, short half‑lives, and the barriers created by suppressive tumor microenvironments. Newer Fc‑silenced, half‑life‑extended designs and better tumor‑specific targets offer promise, especially when BiTEs are combined with other immunotherapies.
Therapeutic targeting of tumour-associated macrophage receptors
DOI: 10.1093/immadv/ltaf009
Rosa Gomes Alves Martins, Mehmet M Tekin, Mark S Cragg, Ali Roghanian
Tumour‑associated macrophages are among the most abundant immune cells in solid tumours, where they help drive cancer growth, spread, and resistance to therapy. This review outlines the most promising TAM‑surface receptors being explored as drug targets, highlighting both their therapeutic potential and the challenges of safely and effectively reprogramming these pro‑tumour immune cells.
Imaging antigen processing and presentation in cancer
DOI: 10.1093/immadv/ltaf002
Doreen Lau, Tim Elliott
Imaging technologies are giving researchers new ways to watch how cancer cells process and present antigens, revealing details of the steps that shape T‑cell activation and immunotherapy outcomes. These tools help map where and how these pathways fail, supporting better biomarker development and improving the ability to predict and monitor treatment responses.
CTLA-4—two pathways to anti-tumour immunity?
Frank J Ward, Paul T Kennedy, Farah Al-Fatyan, Lekh N Dahal, Rasha Abu-Eid
Anti‑CTLA‑4 therapies seem to work through two different mechanisms: either by directly boosting effector T‑cell activity by blocking CTLA‑4 signals, or by depleting regulatory T cells that normally suppress anti‑tumour immunity. This review discusses evidence for both pathways and explores how the soluble form of CTLA‑4 may complicate current treatments while also offering new therapeutic possibilities.
DOI: 10.1093/immadv/ltaf029
Lara V Graham, Ludmila Horehajova, Marco V Haselager, Jack G Fisher, Jamie Lee Roos, Russell B Foxall, Mel John, Kerry L Cox, Robert J Oldham, Martin C Taylor, Margaret Ashton-Key, Ben Sale, Laura G Bartlett, Ali Roghanian, Eric Eldering, Andres F Vallejo, Francesco Forconi, Salim I Khakoo, Mark S Cragg, Matthew D Blunt
CD40L and IL‑4 signals in the lymph node raise HLA‑E levels on malignant B cells, which suppresses NK cell killing by engaging the inhibitory receptor NKG2A and reduces the effectiveness of anti‑CD20 therapy. Blocking NKG2A restores NK‑cell driven antibody-dependent cytotoxicity, suggesting that combining anti‑NKG2A with anti‑CD20 could improve treatment for CLL and lymphoma patients.
Every article you read, cite, or share plays a crucial role in advancing vital research. All revenue generated from our journals is reinvested into BSI initiatives, supporting grants, events, and career development programs that strengthen the immunology community. Your engagement helps drive discovery and ensures continued progress in the field of immunology.
We also encourage you to publish your own research in the BSI journals portfolio, helping to shape the future of immunology. Join the conversation online by tagging us on X, Instagram, LinkedIn, and Bluesky