Journal of Immunology Research最新文献

{"title":"Tfh Cells in Henoch-Schönlein Purpura (IgA Vasculitis): Current Concept.","authors":"Junke Huang, Juan Liu, Yue Hu, Xuan Zhang, Qing Zhang","doi":"10.1155/jimr/4143288","DOIUrl":"10.1155/jimr/4143288","url":null,"abstract":"<p><p>Henoch-Schönlein purpura (HSP) is an inflammatory condition affecting the small blood vessels, leading to organ damage and symptoms across various body systems, including skin, joints, and kidneys. The disease's pathogenesis involves the deposition of immunoglobulin (Ig) A immune complexes in vessels, triggering inflammation and damage. Recent research highlights the role of T follicular helper cells (Tfh cells) in HSP. The review delves into Tfh cells' biological functions, emphasizing their involvement in the HSP's development by activating autoreactive B cells and inducing the production of autoantibodies through the secretion of interleukin (IL)-21, IL-4, and IL-6. Additionally, the roles of different Tfh cell subsets in the pathogenesis of HSP are also characterized by their unique features. We also highlight the relationship between Tfh cells and galactose-deficient IgA1 (Gd-IgA1) production, compare Tfh-mediated immune responses in HSP with those in IgA nephropathy (IgAN) and systemic lupus erythematosus (SLE), and discuss emerging therapeutic strategies targeting the Tfh-B-cell axis. It concludes by suggesting the need for further research on Tfh cells to understand HSP pathogenesis better and develop effective treatments.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e4143288"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endotoxin Tolerance Impinges on T Cell Activation and Chemoattraction in Autoimmune Diabetes.","authors":"Satu M Silojärvi, Linda A A Leino, Sakari A Pöysti, Arno L M Hänninen","doi":"10.1155/jimr/7395567","DOIUrl":"10.1155/jimr/7395567","url":null,"abstract":"<p><p>Gut microbiota may affect the development of autoimmune (type 1) diabetes by differential potency of intestinal species to induce endotoxin tolerance (ET). However, where ET impinges on immune mechanisms underlying autoimmune diabetes is yet incompletely understood. We investigated the effects of lipopolysaccharide (LPS) from E. coli and B. vulgatus, two common intestinal species dominating either in low- or high-incidence countries, on activation and chemoattraction of islet-specific T cells in non-obese diabetic (NOD) mice. Intraperitoneal (i.p.) injection of E. coli LPS induced costimulatory ligands CD40, CD80 and CD86 on both conventional and cross-presenting (XCR1+) dendritic cells (DC) and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-reactive islet-specific T cells in the pancreatic lymph node. In comparison to mice not primed with E. coli LPS or primed with B. vulgatus LPS, the second injection of E. coli LPS lowered the frequency of IGRP-reactive T cells and CD80 expression on DC subsets, as well as CD44 and CD69 activation markers and the CXCR3 chemokine receptor on IGRP-reactive T cells. In islets, expression of chemokine CXCL10 accentuated, and insulitis became more severe in mice primed with B. vulgatus LPS. Our results provide mechanistic insight into how ET affects islet autoimmunity and suggest that physiological exposure to E. coli LPS may benefit in moderating autoimmune diabetes.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e7395567"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2 Receptors as Therapeutic Targets in Allergic Rhinitis: Insights From the Use of Natural Products and Preclinical Studies.","authors":"Thalita Calvet Pereira, Leandro Rocha, Robson Xavier Faria","doi":"10.1155/jimr/7715676","DOIUrl":"10.1155/jimr/7715676","url":null,"abstract":"<p><p>Allergic rhinitis (AR) is a chronic inflammatory disorder of the upper airways that is mediated by immunoglobulin E (IgE) and triggered by environmental allergens. Current pharmacological therapies, including antihistamines, corticosteroids, and immunotherapy, offer symptomatic relief but are limited by their incomplete disease-modulating effects and potential adverse side effects. Purinergic P2 receptors (P2Rs; P2X and P2Y subtypes) have emerged as key modulators of allergic inflammation and regulate mast cell degranulation, T helper 2 (Th2) cytokine release, eosinophil recruitment, and NLRP3 inflammasome activation. Natural products, including polyphenols, flavonoids, terpenoids, and alkaloids, demonstrate multitarget anti-inflammatory effects and have the potential to modulate P2R signaling. However, direct evidence of their activity on P2Rs in AR remains limited. This review critically summarizes the immunopathology of AR, highlights the functional relevance of P2Rs, and discusses emerging natural product-based strategies, emphasizing mechanistic insights and translational potential for the development of novel therapeutics.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e7715676"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13296238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic Arachidonic Acid Dysregulation Impairs Double-Negative Regulatory T Cell-Mediated Immunoregulation via CD39 Downregulation and Drives MASLD Development.","authors":"Hua Jin, Xiyu Wang, Xinjuan Liu, Dong Zhang, Guangyong Sun","doi":"10.1155/jimr/6950401","DOIUrl":"10.1155/jimr/6950401","url":null,"abstract":"<p><p>Immune dysregulation is a key driver of metabolic dysfunction-associated steatotic liver disease (MASLD). Double-negative regulatory T (DNT) cells, which are essential for hepatic immune homeostasis, are functionally impaired in MASLD. CD39, an ectoenzyme that converts ATP to adenosine, sustains DNT cell viability and immunoregulatory function. However, the mechanisms of MASLD-induced CD39 dysregulation remain unknown. In this study, a transcriptomic analysis of hepatic DNT cells from MASLD mice revealed reduced ATP hydrolysis, as confirmed by flow cytometry, and lower CD39 level compared to normal control diet-fed mice. Similarly, single-cell transcriptomic data showed that CD39 was downregulated in hepatic DNT cells from MASLD patients, and higher CD39 expression was associated with enhanced cytotoxicity and viability. Furthermore, in vitro experiments confirmed that CD39 maintained the immunosuppressive function of DNT cells by hydrolyzing ATP and suppressing monocyte activation. Mechanistically, arachidonic acid (AA), which is enriched in the livers of MASLD, suppressed CD39 via hypoxia-inducible factor-1α (HIF-1α). This AA-HIF-1α-CD39 axis impaired DNT cell-mediated monocyte immunosuppression, accelerating immune imbalance and MASLD progression. These findings establish the AA-HIF-1α-CD39 axis as a key pathway driving DNT cell dysfunction in MASLD, highlighting potential therapeutic strategies targeting metabolic-immune crosstalk to restore hepatic immune balance.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e6950401"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13296590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mucosal Immunity: The Key to Combating Enteroviruses and Beyond.","authors":"Nida Kalam, Vinod R M T Balasubramaniam","doi":"10.1155/jimr/4856137","DOIUrl":"10.1155/jimr/4856137","url":null,"abstract":"<p><p>Enteroviruses (EVs) lead to 10-15 million symptomatic infections each year in the United States alone. EVs enter through either the gastrointestinal or respiratory mucosa, depending on the specific virus. Since these mucosal surfaces are the primary entry points for viruses, mucosal immunity serves as a crucial first line of defense. Nevertheless, the mechanisms that drive it are poorly understood for most EVs. Conventional intramuscular vaccines provide limited protection at these sites, leaving them unprotected; mucosal vaccination addresses this issue directly by generating local SIgA in GALT/NALT that neutralizes pathogens before they spread systemically, while also offering advantages in accessibility and cost. This is not merely theoretical; oral vaccines for polio and rotavirus have already shown the effectiveness of mucosal immunization at scale for enteric viral diseases. This review explores innate pattern recognition through TLR3, RIG-I, and MDA5 pathways, type I/III interferon (IFN) signaling, and mucosal SIgA responses across key EVs. It also assesses current mucosal vaccine candidates for EV-A71, CVA16, and EV-D68, most of which remain in preclinical stages. Understanding of these mechanistic gaps is important for advancing successful mucosal vaccine strategies into effective next-generation vaccines for EVs.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e4856137"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13486970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial Profiling and Prognostic Role of CD169+ Macrophages in Colorectal Cancer From Adjacent Nontumor Mucosa to Liver Metastasis.","authors":"Wenjing Ye, Sergii Pavlov, Esraa Ali, Filip Ambrozkiewicz, Lenka Červenková, Ondřej Vyčítal, Petr Hošek, Ondřej Daum, Václav Liška, Kari Hemminki, Andriy Trailin","doi":"10.1155/jimr/7305785","DOIUrl":"10.1155/jimr/7305785","url":null,"abstract":"<p><strong>Background: </strong>CD169+ cells represent a distinct subset of macrophages with potential immunomodulatory roles, but their function in colorectal cancer (CRC) progression remains unclear. This study focuses on the spatial profiling and prognostic significance of CD169+ macrophages in adjacent nontumor mucosa (NM), primary CRC (pCRC), and synchronous or metachronous liver metastases (LM).</p><p><strong>Materials and methods: </strong>We enrolled into this retrospective cohort study patients who underwent resection of both pCRC with adjacent NM and synchronous LM (N = 55) or metachronous LM (N = 44). We applied immunohistochemical staining and computer-assisted image analysis to quantify CD169+ cell density in the NM, pCRC, synchronous, and metachronous LM. Correlations between CD169+ macrophages and T cells were evaluated. Associations between CD169+ cell density and overall survival (OS) of the patients were assessed.</p><p><strong>Results: </strong>CD169+ cell density was greater in NM than in the tumor center (TC) of pCRC and in the peritumor (PT) region of LM compared to pCRC. The synchronous group exhibited a higher density of CD169+ cells than the metachronous group in the inner margin (IM) of pCRC, the TC, and the outer margin (OM) of LM. CD169+ cells were more abundant in the exterior than in the interior tumor areas in both pCRC and LM. Positive correlations were observed between densities of CD169+ macrophages with CD3+ and CD8+ lymphocytes. In the synchronous group, a high density of CD169+ macrophages in the TC of pCRC was associated with longer OS, whereas a high density in the PT of LM was associated with shorter OS. High density of CD169+ macrophages in the OM of metachronous LM was associated with poor survival.</p><p><strong>Conclusion: </strong>Our study highlights context-dependent prognostic associations of CD169+ macrophages in CRC. While high CD169+ macrophage density in the TC of pCRC was linked to favorable survival in the synchronous group, increased density in both synchronous and metachronous LM was associated with adverse outcomes. Further prospective studies and functional investigations are needed to validate these observations.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e7305785"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fucoxanthin Ameliorates Diabetic Kidney Disease via Modulating the Gut Microbiota and Tryptophan-Kynurenine Metabolic Pathway.","authors":"Donglin Guo, Jiayong Xie, Xueyun Dong, Hao Xu, Yunhan Xie, Xinyu Liu, Linlin Xu, Asmaa Ali, Min Chen, Leilei Zhang, Jiayuan He, Liang Wu, Keke Shao","doi":"10.1155/jimr/1020462","DOIUrl":"10.1155/jimr/1020462","url":null,"abstract":"<p><p>This study employs a multiomics approach to investigate the protective effects of fucoxanthin (Fu) and explore its potential association with metabolic and signaling pathways in diabetic mice induced by a high-fat diet combined with streptozotocin (STZ) administration. Diabetic model mice were randomly divided into normal control (NC), diabetic model, low-dose Fu (50 mg/kg/day), and high-dose Fu (100 mg/kg/day) groups. After 6 weeks of intervention, Fu treatment was associated with dose-dependent improvements in glucose and lipid metabolism, reduced oxidative stress, decreased expression of inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and IL-1β) and renal fibrosis markers (TGF-β1, α-SMA, and Col1a1), along with notable attenuation of renal pathological damage. Exploratory analyses indicated that these phenotypic improvements were accompanied by reduced renal IDO1 expression, favorable shifts in tryptophan (Trp) metabolism, and upregulated AhR/CYP1A1 signaling. 16S rRNA sequencing revealed that Fu treatment was associated with a restoration of diabetes-altered gut microbiota β-diversity. Serum metabolomics identified that Fu administration correlated with alterations in multiple metabolites (including 5'-S-methyl-5'-thioadenosine, LPC 16:0, and bile acids), which are linked to key pathways such as Trp metabolism and bile acid biosynthesis. Network pharmacology predictions further suggested potential multitarget interactions of Fu with the PI3K-Akt and AGE-RAGE signaling pathways. Collectively, these findings indicate that Fu exerts potential renoprotective effects in diabetic mice, which are accompanied by a normalization of Trp-AhR pathway-related metabolism and concurrent attenuation of inflammatory, oxidative, and fibrotic responses. While causal functional links remain to be fully elucidated, these observations provide a preliminary basis for further mechanistic investigation and support the potential of Fu as a dietary supplement or adjunctive strategy for diabetic kidney disease (DKD).</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1020462"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13575650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148969324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Scar-Associated Macrophages in Organ Fibrosis Diseases.","authors":"Runmin Ding, Zexin Yang, Yuxi Chen, Qiqin Yu, Yisheng Ji, Zijie Wang, Min Gu","doi":"10.1155/jimr/8393673","DOIUrl":"10.1155/jimr/8393673","url":null,"abstract":"<p><p>Fibrosis refers to the scarring and hardening of tissue resulting from the excessive deposition of extracellular matrix (ECM) proteins by myofibroblasts during chronic inflammatory responses, which can ultimately lead to organ failure and potentially death. Different states of macrophage activation are critical in regulating both the progression and regression of fibrosis. However, the conventional M1/M2 polarization model fails to accurately capture the dynamic and heterogeneous states of macrophages observed in vivo. As a result, an increasing number of studies have begun to classify macrophages based on their functional phenotypes. One specific subset of functionally distinct macrophages, termed scar-associated macrophages (SAMs), has been confirmed to play a significant regulatory role in organ fibrosis. This review provides a comprehensive summary of recent advances in understanding the role of SAMs in fibrotic diseases across multiple organs, including the liver, lungs, heart, and kidneys. It further explores the emerging conceptual framework of hot and cold fibrosis, highlighting the potential role of SAMs as central cellular mediators that sustain a positive feedback loop between inflammation and fibrosis in the \"hot fibrosis\" state. Building on these insights, this review also discusses future research directions aimed at developing targeted therapeutic strategies to modulate SAM activity and mitigate fibrosis in diverse organ systems.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e8393673"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combining Activation-Induced Markers With PD-L1 Selectively Enhances Detection of Antigen-Specific T Cells in Virus-Infected Individuals.","authors":"Christine Kreher, Laura Y L Kummer, Maryse Tempert, Veronique A L Konijn, Gertjan Wolbink, Filip Eftimov, Taco W Kuijpers, Theo Rispens, S Marieke van Ham, Anja Ten Brinke","doi":"10.1155/jimr/1284907","DOIUrl":"10.1155/jimr/1284907","url":null,"abstract":"<p><p>Detection and characterization of antigen-specific T cells are important for studying immune responses upon infection, vaccination, or autoreactivity. The activation-induced marker (AIM) assay is a robust technique to identify and characterize antigen-specific CD4 and CD8 T cells. However, there is variability in the AIM assay, particularly in the type and number of activation markers used. In this study, we set out to define which marker combinations are most suited to optimally detect antigen-specific CD4 and CD8 T cells and if certain marker combinations preferentially detect specific CD4 T helper subsets. A multiparameter flow cytometry panel, including six common activation markers: CD40L, CD137, CD69, OX40, CD25, and PD-L1, was used for detecting antigen-specific T cells following infection (SARS-CoV-2 and CMV) or vaccination (mRNA-1273 SARS-CoV-2). We demonstrate that combining multiple activation markers increases the detection frequency of antigen-specific CD4 T cells compared to commonly used dual marker combinations. In addition, marker combinations including PD-L1 detected a higher frequency of antigen-specific CD4 T cells in SARS-CoV-2 and CMV infected but not in SARS-CoV-2-vaccinated individuals. Certain dual marker combinations preferentially detected specific CD4 T helper subsets. The majority of antigen-specific CD8 T cells were captured by the dual combination of CD69 plus CD25. In conclusion, combining CD137, CD69, OX40, CD25, and PD-L1 in an AIM assay results in robust and optimal detection of both specific CD4 T helper subsets and CD8 T cells in different antigenic contexts.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1284907"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and Validation of a Multiplex Flow Cytometry-Based PBMC Assay for Immunomodulator Screening.","authors":"Regine Brox, Holger Hackstein","doi":"10.1155/jimr/5535208","DOIUrl":"10.1155/jimr/5535208","url":null,"abstract":"<p><p>The identification of novel compounds capable of stimulating or suppressing immune responses is critical for advancing immunotherapy and improving our understanding of immune regulation. However, traditional screening approaches are often limited by low throughput, poor physiological relevance, and insufficient resolution to detect subtle immunomodulatory effects. In this study, we introduce a validated and robust multiplexed flow cytometry-based functional screening assay that enables efficient and precise identification of immunomodulatory compounds, while addressing the key limitations of conventional methods. By using human peripheral blood mononuclear cells (PBMCs) and defined stimulation conditions, the assay mimics complex immune interactions in a physiologically relevant context. It simultaneously monitors T- and B-cell responses across multiple functional readouts, including T-cell proliferation (carboxyfluorescein succinimidyl ester [CFSE]), activation (CD25, CD71), and B-cell costimulatory marker expression (CD86), enabling an in-depth assessment of immune modulation within heterogenous cell populations. The incorporation of robust statistical validation using the Z-factor further supports assay reliability and reproducibility. In a pilot screen with 295 immunology-related compounds, the assay demonstrated its ability to identify known immunomodulators with distinct functional profiles. This multiplex functional screening approach bridges the gap between mechanistic immunology and drug discovery by enabling systematic identification and characterization of immunotherapeutic candidates, while providing new insights into the complex dynamics of immune regulation.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5535208"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13434440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}