Immunotherapy advancesPub Date : 2025-04-20eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf003
Aqsa Bibi, Zhenjiang Yu, Lv Cui, Guiwen Yang
{"title":"Harnessing monocyte dynamics for treatment of multiple sclerosis; insights from experimental model studies.","authors":"Aqsa Bibi, Zhenjiang Yu, Lv Cui, Guiwen Yang","doi":"10.1093/immadv/ltaf003","DOIUrl":"https://doi.org/10.1093/immadv/ltaf003","url":null,"abstract":"<p><p>Monocytes are central to the innate immune system's response to infection or injury. In murine, these cells are classified into distinct subsets: classical monocytes, defined by elevated Ly6C expression (Ly6C<sup>hi</sup>), intermediate monocytes (Ly6C<sup>int</sup>), and non-classical inflammatory monocytes, characterized by low Ly6C expression (Ly6C<sup>low</sup>). Monocytes recruited to tissues differentiate into macrophages, which can be pro-inflammatory or anti-inflammatory, thereby influencing disease processes and outcomes. The principal function of classical monocytes is the mediation of pro-inflammatory reactions, whereas non-classical monocytes are associated with repair and anti-inflammatory processes, patrolling the lumen of the vessels. Growing evidence highlights the importance of monocytes in multiple sclerosis (MS), an autoimmune and neurodegenerative disease of the central nervous system (CNS). Recent studies indicate that modulation of the innate immune system, focusing specifically on the shift from Ly6C<sup>hi</sup> to Ly6C<sup>low</sup> monocytes, is an effective therapeutic strategy for neurodegenerative diseases, such as Alzheimer's and MS. This transition is crucial for switching the immune response from inflammation to tissue repair and inflammation resolution, emphasizing the plasticity of monocytes and their potential as targets in MS. This review differs from prior studies in that it focuses solely on animal models of MS, which either directly perturb or study monocytes, or where therapeutic approaches mediate their protective effects through monocytes. Such details permit a subtle comprehension of monocyte dynamics in the context of MS.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf003"},"PeriodicalIF":4.1,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144030323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunotherapy advancesPub Date : 2025-03-28eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf015
Lozan Sheriff, Alastair Copland, David A J Lecky, Reygn Done, Lorna S George, Emma K Jennings, Sophie Rouvray, Thomas A E Elliot, Elizabeth S Jinks, Lalit Pallan, David Bending
{"title":"Lag3 and PD-1 pathways preferentially regulate NFAT-dependent TCR signalling programmes during early CD4<sup>+</sup> T cell activation.","authors":"Lozan Sheriff, Alastair Copland, David A J Lecky, Reygn Done, Lorna S George, Emma K Jennings, Sophie Rouvray, Thomas A E Elliot, Elizabeth S Jinks, Lalit Pallan, David Bending","doi":"10.1093/immadv/ltaf015","DOIUrl":"https://doi.org/10.1093/immadv/ltaf015","url":null,"abstract":"<p><strong>Introduction: </strong>Lag3 and PD-1 are immune checkpoints that regulate T cell responses and are current immunotherapy targets. Yet how they function to control early stages of CD4<sup>+</sup> T cell activation remains unclear.</p><p><strong>Methods: </strong>Here, we show that the PD-1 and Lag3 pathways exhibit layered control of the early CD4<sup>+</sup> T cell activation process, with the effects of Lag3 more pronounced in the presence of PD-1 pathway co-blockade (CB). RNA sequencing revealed that CB drove an early NFAT-dependent transcriptional profile, including promotion of ICOS<sup>hi</sup> T follicular helper cell differentiation.</p><p><strong>Results: </strong>NFAT pathway inhibition abolished CB-induced upregulation of NFAT-dependent co-receptors ICOS and OX40, whilst unaffecting the NFAT-independent gene <i>Nr4a1</i>. Mechanistically, Lag3 and PD-1 pathways functioned additively to regulate the duration of T cell receptor signals during CD4<sup>+</sup> T cell re-activation. Phenotypic changes in peripheral blood CD4<sup>+</sup> T cells in humans on anti-Lag3 and anti-PD-1 combination therapy revealed upregulation of genes encoding ICOS and OX40 on distinct CD4<sup>+</sup> T cell subsets, highlighting the potential translational relevance of our findings.</p><p><strong>Conclusion: </strong>Our data therefore reveal that PD-1 and Lag3 pathways converge to additively regulate TCR signal duration and may preferentially control NFAT-dependent transcriptional activity during early CD4<sup>+</sup> T cell re-activation.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf015"},"PeriodicalIF":4.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12066006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144037625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Abnormal glucose and lipid metabolism promotes disrupted differentiation of T and B cell subsets in Behçet's disease.","authors":"Minghao Li, Ping Li, Xin Wang, Lijie Wang, Guanmin Gao, Guosheng Jiang, Tingting Liu, Wei Lin","doi":"10.1093/immadv/ltaf010","DOIUrl":"https://doi.org/10.1093/immadv/ltaf010","url":null,"abstract":"<p><strong>Introduction: </strong>Behçet's disease (BD) is a chronic, systemic inflammatory condition characterized by recurrent immune dysregulation.</p><p><strong>Materials & methods: </strong>This study conducted a comprehensive analysis of immune cell subsets, metabolic markers, and their interplay in BD patients. Using multiparametric flow cytometry, we identified elevated Th1 cells, senescent CD8<sup>+</sup> T cells, and abnormal B cell activation as hallmarks of the chronic inflammatory state in BD.</p><p><strong>Results: </strong>Despite immunotherapy, innate immune activation persisted, with increased mature NK cells, γδT1 cells, and conventional dendritic cells (cDCs), alongside reduced plasmacytoid dendritic cells (pDCs). Elevated glucose (GLU) and triacylglycerol (TAG) levels in BD patients correlated with increased Th1 cells, functional CD8<sup>+</sup> T cells, and B cell activation. In vitro experiments demonstrated that GLU and TAG promote Th1 differentiation, CD8<sup>+</sup> T cell activation, and B cell antibody production, revealing their role as drivers of immune dysregulation.</p><p><strong>Conclusion: </strong>These findings underscore the intricate relationship between metabolic dysregulation and immune dysfunction in BD, highlighting potential diagnostic and therapeutic targets. Our study provides critical insights into BD pathogenesis, offering a foundation for optimizing disease management and monitoring immune and metabolic markers for improved patient outcomes.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf010"},"PeriodicalIF":4.1,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144054531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunotherapy advancesPub Date : 2025-03-17eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf011
Radwa Fawzy Ahmed, Paul Fenton, Adityanarayan Bhatnagar, Victoria Wood, Andrew Bates
{"title":"Implementing adjuvant immunotherapy following radical chemoradiotherapy for stage III non-small-cell lung cancer in UK clinical practice-Are the PACIFIC trial outcomes achievable in the real world?","authors":"Radwa Fawzy Ahmed, Paul Fenton, Adityanarayan Bhatnagar, Victoria Wood, Andrew Bates","doi":"10.1093/immadv/ltaf011","DOIUrl":"https://doi.org/10.1093/immadv/ltaf011","url":null,"abstract":"<p><strong>Introduction: </strong>PACIFIC trial demonstrates improved progression-free survival (PFS) and overall survival (OS) in patients with locally advanced non-small-cell lung cancer (NSCLC) treated with platinum-based concurrent chemoradiotherapy (CRT) and adjuvant Durvalumab immunotherapy.</p><p><strong>Methods: </strong>We retrospectively reviewed 72 consecutive patients with locally advanced NSCLC treated with platinum-based concurrent CRT, who were potentially eligible for adjuvant Durvaluamb treatment (PDL1 ≥1% or inadequate). We analysed PFS, OS, treatment toxicity, and the impact of PDL1 on these outcomes.</p><p><strong>Results: </strong>The cohort median follow-up was 20 months. Fifty-five patients received adjuvant Durvalumab. The median OS (mOS) has not been reached. OS at 24 months was 67.8% for patients received Durvalumab. The median PFS (mPFS) for patients received Durvalumab was 30 months. PDL1 status (1-49% vs. ≥50%) did not affect outcome in our cohort. Sixteen patients stopped Durvalumab due to immune toxicity. At 24 months, 49% of these patients were still alive versus 76% of the patients who completed 12 months of treatment. The mOS for patients who stopped Durvalumab due to immune toxicity was 16 months, <i>P</i> = .0032. Seventeen patients did not receive adjuvant treatment due to insufficient performance status following CRT and mOS was 6 months.</p><p><strong>Conclusions: </strong>Our real-world experience demonstrates possibility to achieve similar outcomes to PACIFIC trial. PDL1 status did not affect clinical outcome in our cohort. Patients who stopped adjuvant Durvalumab treatment due to toxicity and those who were not deemed suitable to proceed with adjuvant Durvalumab after CRT, had poorer outcomes. This indicates that careful case selection remains essential.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf011"},"PeriodicalIF":4.1,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12076069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunotherapy advancesPub Date : 2025-03-12eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf006
Louis Waeckel, Chloé Talon, Mathilde Barrau, Anne-Emmanuelle Berger, Xavier Roblin, Stéphane Paul
{"title":"Development and evaluation of two whole-blood flow cytometry protocols for monitoring patients treated with JAK inhibitors.","authors":"Louis Waeckel, Chloé Talon, Mathilde Barrau, Anne-Emmanuelle Berger, Xavier Roblin, Stéphane Paul","doi":"10.1093/immadv/ltaf006","DOIUrl":"https://doi.org/10.1093/immadv/ltaf006","url":null,"abstract":"<p><strong>Introduction: </strong>The clinical efficacy of Janus kinase inhibitors (JAKinibs) is highly variable and their safety profiles are poorly understood.</p><p><strong>Methods: </strong>We established two flow cytometry panels for the assessment of two promising leukocyte biomarkers: signal transducer and activator of transcription (STAT) phosphorylation and cytokine receptor expression. We evaluated the first panel, which assesses phosphorylation levels for STAT1, STAT3, and STAT5 after cytokine stimulation, with or without <i>in vitro</i> pretreatment with JAKinibs, in 10 healthy donors. We then evaluated the second panel, which assesses cytokine receptor expression on T cells and B cells, in five healthy donors.</p><p><strong>Results: </strong>Stimulation with interleukin (IL)-2 or IL-7 increased STAT5 phosphorylation in T cells but not in B cells or monocytes. IL-6 stimulation induced STAT3 phosphorylation in monocytes and CD4 T cells and, to a lesser extent, in CD8 T cells, but not in B cells. IL-21 stimulation led to STAT3 phosphorylation in T cells and, to a lesser extent, in B cells, but not in monocytes. Interferon-α stimulation increased STAT1 phosphorylation in all cell types. STAT phosphorylation levels were lower after pretreatment with JAKinibs. A dose-response curve was plotted, confirming the correlation between JAKinib concentration and STAT phosphorylation inhibition. The second panel showed that each cell type displayed a distinct pattern of cytokine receptors expression, and that this pattern might be modified by <i>in vitro</i> treatment with JAKinibs.</p><p><strong>Conclusion: </strong>This preliminary study confirms the utility of flow cytometry for monitoring the biological effects of JAKinibs. Further studies on treated patients are now required to evaluate the clinical value of these two flow cytometry panels.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf006"},"PeriodicalIF":4.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144037622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"M2 macrophages promote IL-10<sup>+</sup>B-cell production and alleviate asthma in mice.","authors":"Baichao Yu, Xueqi Wang, Yongkun Zheng, Wenjun Wang, Xiaoqin Cheng, Yue Cao, Mingxing Wei, Ying Fu, Yiwei Chu, Luman Wang","doi":"10.1093/immadv/ltaf007","DOIUrl":"https://doi.org/10.1093/immadv/ltaf007","url":null,"abstract":"<p><strong>Introduction: </strong>B cells have a central regulatory role in various diseases. While macrophages are found in the disease microenvironment and interact with tissue and diverse immune cells, their relationship with B cells remains poorly explored.</p><p><strong>Methods: </strong>This study used an asthma animal model and macrophage depletion and demonstrated a significant exacerbation of asthma symptoms upon macrophage removal, coupled with a marked reduction in IL-10<sup>+</sup> B-cell expression.</p><p><strong>Results: </strong>Further analysis revealed that the macrophages interacting with IL-10<sup>+</sup> B cells in the asthma microenvironment were of the M2 subtype. Furthermore, our sequencing data indicated a potential mechanism wherein M2 macrophages promote IL-10<sup>+</sup> B-cell activity through the TGF-β pathway and oxidative phosphorylation pathways.</p><p><strong>Conclusion: </strong>These findings suggest that M2 macrophages modulate IL-10<sup>+</sup> B cells, ultimately mitigating asthma symptoms in mouse models.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf007"},"PeriodicalIF":4.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunotherapy advancesPub Date : 2025-03-07eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf008
Frank J Ward, Paul T Kennedy, Farah Al-Fatyan, Lekh N Dahal, Rasha Abu-Eid
{"title":"CTLA-4-two pathways to anti-tumour immunity?","authors":"Frank J Ward, Paul T Kennedy, Farah Al-Fatyan, Lekh N Dahal, Rasha Abu-Eid","doi":"10.1093/immadv/ltaf008","DOIUrl":"https://doi.org/10.1093/immadv/ltaf008","url":null,"abstract":"<p><p>Immune checkpoint inhibitor (ICI) therapies have revolutionized cancer therapy and improved patient outcomes in a range of cancers. ICIs enhance anti-tumour immunity by targeting the inhibitory checkpoint receptors CTLA-4, PD-1, PD-L1, and LAG-3. Despite their success, efficacy, and tolerance vary between patients, raising new challenges to improve these therapies. These could be addressed by the identification of robust biomarkers to predict patient outcome and a more complete understanding of how ICIs affect and are affected by the tumour microenvironment (TME). Despite being the first ICIs to be introduced, anti-CTLA-4 antibodies have underperformed compared with antibodies that target the PD-1/PDL-1 axis. This is due to the complexity regarding their precise mechanism of action, with two possible routes to efficacy identified. The first is a direct enhancement of effector T-cell responses through simple blockade of CTLA-4-'releasing the brakes', while the second requires prior elimination of regulatory T cells (T<sub>REG</sub>) to allow emergence of T-cell-mediated destruction of tumour cells. We examine evidence indicating both mechanisms exist but offer different antagonistic characteristics. Further, we investigate the potential of the soluble isoform of CTLA-4, sCTLA-4, as a confounding factor for current therapies, but also as a therapeutic for delivering antigen-specific anti-tumour immunity.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf008"},"PeriodicalIF":4.1,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunotherapy advancesPub Date : 2025-02-24eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf005
Akhilesh Jha, Marie Fisk, Jamie Forrester, Jacqui Galloway, Jade Joseph, Robyn Staples, Karl P Sylvester
{"title":"Lung immune challenge study protocol: controlled exposure to inhaled resiquimod (R848) to study mechanisms of inflammation.","authors":"Akhilesh Jha, Marie Fisk, Jamie Forrester, Jacqui Galloway, Jade Joseph, Robyn Staples, Karl P Sylvester","doi":"10.1093/immadv/ltaf005","DOIUrl":"10.1093/immadv/ltaf005","url":null,"abstract":"<p><p>This study aims to develop a human lung immune challenge model using inhaled Resiquimod (R848), a Toll-like receptor 7/8 agonist, to investigate inflammatory mechanisms involved in the human respiratory mucosa in health and disease. This approach seeks to induce innate immune anti-viral responses in the lungs and blood, with a suitable dose of inhaled R848 that is clinically tolerable. The study will include healthy volunteers and individuals with asthma. The primary outcome is a change in CXCL10, a biomarker representative of anti-viral responses, at 24 hours post-exposure. Secondary outcomes include changes in lung function, physiological parameters, and inflammatory markers, including C-reactive protein and eosinophil counts. This trial involves a single ascending dose, randomized, single-blind, placebo-controlled design. Participants will receive R848 via nebulization in escalating doses from 0.1 to 100 µg/ml or saline placebo. Safety assessments include spirometry, vital signs, and blood samples to monitor systemic and lung-specific immune responses. The study will contribute to understanding immune pathways in asthma and provide a platform for testing novel anti-inflammatory therapeutics. The protocol has been approved by relevant ethics committees and will be disseminated via peer-reviewed publications and open-access data repositories.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf005"},"PeriodicalIF":4.1,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11976720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143812981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunotherapy advancesPub Date : 2025-02-08eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf004
Helen R Wagstaffe, Stephanie Ascough, Peter J M Openshaw
{"title":"Human challenge models for vaccine development-strengths, limitations, and expansion into endemic settings: a HIC-Vac meeting report.","authors":"Helen R Wagstaffe, Stephanie Ascough, Peter J M Openshaw","doi":"10.1093/immadv/ltaf004","DOIUrl":"https://doi.org/10.1093/immadv/ltaf004","url":null,"abstract":"<p><p>The HIC-Vac network is a unique association of researchers focussed on the development and use of human infection challenge (HIC, otherwise known as controlled human infection models or CHIM) studies for vaccine and therapeutic development, particularly for pathogens of high global impact. The fifth annual meeting of the HIC-Vac network was held on 1-3 November 2023. The theme of the meeting was capacity-building in endemic settings particularly in low- and middle-income countries (LMIC), where pathogens cause the greatest morbidity and mortality. In this report we highlight the strengths and limitations of HIC and expansion of such studies into endemic settings, noting that immune responses and vaccine efficacy differ across diverse settings and populations. The consensus was that HIC studies must not be restricted to high income settings if they are to be relevant to LMIC populations. This report summarizes the work presented at the HIC-Vac annual meeting, highlighting current and future challenge models, challenge agent manufacture, public engagement, ethics, and industry perspectives.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf004"},"PeriodicalIF":4.1,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144013922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunotherapy advancesPub Date : 2025-02-04eCollection Date: 2025-01-01DOI: 10.1093/immadv/ltaf002
Doreen Lau, Tim Elliott
{"title":"Imaging antigen processing and presentation in cancer.","authors":"Doreen Lau, Tim Elliott","doi":"10.1093/immadv/ltaf002","DOIUrl":"https://doi.org/10.1093/immadv/ltaf002","url":null,"abstract":"<p><strong>Introduction: </strong>Antigen processing and presentation are vital processes of the adaptive immunity. These processes involve a series of intracellular and extracellular events, including the enzymology within cells during antigen processing, the loading and presentation of antigenic peptides on major histocompatibility complexes, the recruitment of T cells, their interaction with antigen-presenting cells, and the expression of adhesion, co-stimulatory and co-inhibitory molecules at the T cell immunological synapse. These events collectively fine-tune and sustain antigen recognition and T cell function. Dysregulation of this machinery can profoundly impact the efficacy of cancer immunotherapy. Imaging technologies have emerged as powerful tools for elucidating the mechanisms underlying antigen processing and presentation. By providing complementary perspectives into the cellular and molecular interactions at play, imaging has significantly enhanced our understanding of these complex immunological events in cancer. Such insights can improve the monitoring of immunotherapy responses, facilitate the identification of effective treatments, and aid in predicting patient outcomes.</p><p><strong>Methods: </strong>This review explores the role of imaging in studying antigen processing and presentation in the context of cancer.</p><p><strong>Conclusion: </strong>It highlights key considerations for developing imaging tools and biomarkers to detect components of these pathways. Additionally, it examines the strengths and limitations of various imaging approaches and discusses their potential for clinical translation.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf002"},"PeriodicalIF":4.1,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144059204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}