Journal of Immunology Research最新文献

{"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}

{"title":"A Hidden Checkpoint: Bidirectional pH Remodeling of the Immunological Synapse in Cancer, Methods, and Therapeutic Opportunities.","authors":"Aurélie Guillemette, Eva Gez, Sofia Titah, Yasmine Touil","doi":"10.1155/jimr/5768926","DOIUrl":"10.1155/jimr/5768926","url":null,"abstract":"<p><p>The immunological synapse (IS) is a nanoscale platform that coordinates T cell activation, cytoskeletal polarization, Ca²⁺ signaling, and the directed secretion of lytic granules. In cancers, an acidic tumor microenvironment (TME; extracellular pH_e ~ 6.4-6.8) imposes a biophysical and metabolic stress that could destabilize this interface. Experimental studies indicate that even modest acidification could significantly reduce integrin-dependent adhesion strength, delay actin clearance at the synapse, and suppress store-operated Ca²⁺ entry, thereby leading to marked decreases in cytokine production and cytotoxic granule release. In parallel, tumor cells often maintain relative intracellular alkalinity by enhancing proton export via transporters such as NHE1, MCT1/4, and CAIX, thereby reinforcing cortical actin \"shielding,\" metabolic resilience, and resistance to perforin-mediated killing. These asymmetric pH adaptations may therefore establish a hidden checkpoint at the IS that favors tumor survival. We synthesize current evidence on pH-dependent regulation of actin dynamics, integrin activation, mitochondrial function, and Ca²⁺ channels (Orai1/STIM1); highlight key methodological gaps, including the lack of approaches combining real-time intra- and extracellular pH and Ca²⁺ imaging; and discuss enabling technologies such as microfluidic platforms, genetically encoded pH sensors, and multiparametric single-cell assays. Finally, we outline therapeutic strategies aimed at modulating pH (buffers, inhibitors of NHE1, MCTs, V-ATPases, or CAIX) or engineering pH-resistant effector cells and consider how these approaches could synergize with immune checkpoint blockade, CAR-T cells, and bispecific antibodies. Viewing acidosis as a druggable checkpoint reframes the IS as a bidirectional, pH-tuned system and suggests testable paths to restore antitumor immunity.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5768926"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13128168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773438","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":"Piplartine as an Innovative Natural Product With Dual Antiparasitic and Immunomodulatory Actions.","authors":"Lucas Fukui-Silva, Felipe C R de Souza, Camila S Amorim, Josué de Moraes","doi":"10.1155/jimr/9793044","DOIUrl":"10.1155/jimr/9793044","url":null,"abstract":"<p><p>Neglected tropical diseases (NTDs) remain a major global health burden, disproportionately affecting low- and middle-income regions and demanding innovative therapeutic strategies. This review summarizes current evidence on piplartine (piperlongumine), a naturally occurring amide from Piper species with broad antiparasitic and immunomodulatory properties. Studies on Schistosoma mansoni, Angiostrongylus cantonensis, Leishmania spp., Trypanosoma cruzi, Trypanosoma brucei, Plasmodium falciparum, and Toxoplasma gondii demonstrate potent activity at micromolar levels, associated with disruption of parasite redox homeostasis. In host immune cells, piplartine modulates NF-κB and Nrf2 signaling, inhibits the immunoproteasome, and promotes antioxidant and anti-inflammatory responses. These dual properties suggest that piplartine may influence both parasite survival and host immunopathology through redox-sensitive mechanisms, although direct cause-effect relationships during parasitic infection remain to be experimentally established. The compound's favorable drug-likeness, oral bioavailability, and selective toxicity profile highlight its potential as a multitarget scaffold for the development of next-generation therapeutics against neglected tropical and immune-related diseases.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e9793044"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140805/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433250","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":"Mitochondrial Transcription Factor A Deficiency in T Cells Leads to Activation of the Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase/Stimulator of Interferon Genes Pathway and Production of Autoantibodies in Mice.","authors":"Shuhei Mashimo, Taku Kuwabara, Kei Ito, Tetuo Mikami, Akira Ishiko, Motonari Kondo","doi":"10.1155/jimr/2594317","DOIUrl":"10.1155/jimr/2594317","url":null,"abstract":"<p><p>Mitochondrial transcription factor A (TFAM) is a key regulator of mitochondrial DNA transcription and replication. T cell-specific TFAM-deficient mice are immunocompromised, often succumbing to viral infection, and their T cells are unresponsive to T-cell antigen receptor (TCR) stimulation, suggesting that TFAM-mediated mitochondrial activity regulates T-cell activity, such as effector function and memory formation. In contrast to the attenuation of immune response, TFAM deficiency may also induce inflammatory responses, raising the possibility that TFAM deficiency results in inflammation-mediated autoimmune responses. Thus, besides regulating T-cell function, TFAM plays important roles in autoimmune responses. However, its role in autoimmune diseases remains uncertain. We aimed to investigate the role of TFAM in autoimmune diseases using T cell-specific TFAM-deficient mice. We detected anti-double-strand (ds) DNA antibody, and interferon alpha (IFNα) and IFNγ in the serum of TFAM^fl/fl CD4Cre mice after 30 weeks of age. Mononuclear cell infiltration was observed in the kidneys. TFAM-deficient T cells exhibited leakage of mitochondrial DNA into the cytoplasm. Cytoplasmic mitochondrial DNA was associated with activation of TANK-binding kinase 1 (TBK1) and IFN regulatory factor 3 (IRF3)-the downstream molecules of the nucleic acid sensor cyclic guanosine monophosphate-adenosine monophosphate synthase/stimulator of IFN genes (cGAS/STING) machinery. mRNA expression of type I IFN genes was elevated in T cells from TFAM^fl/fl CD4Cre mice. The suppressive function of Foxp3⁺ regulatory T (Treg) cells, which play a major role in establishment of peripheral tolerance, was reduced in the absence of TFAM. Our findings suggest that T cells in TFAM-deficient conditions may contribute to immune instability and autoimmune responses by inducing type I IFN-mediated inflammatory responses.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e2594317"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13358363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430559","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":"Impact of Transport Media on IL-33 Levels in Samples From Patients With Viral Respiratory Infections.","authors":"Daniela Moreno-Tapia, Yaneisi Vázquez, Valentina Pavez, Omar P Vallejos, José Acevedo-López, Camila Pardo, Felipe A Cancino, Ana María Contreras, Marcela Ferrés, Dona Benadof, Ana María Guzmán, Francisca Valdivieso, Mauricio Farfán, María Luisa Rioseco, Valentina Gutiérrez, Pablo J Bertrand, Eduardo Espejo, Angélica Domínguez, Cecilia V Tapia, Pablo A González, Hernán F Peñaloza, Alexis M Kalergis, Susan M Bueno","doi":"10.1155/jimr/3274290","DOIUrl":"10.1155/jimr/3274290","url":null,"abstract":"<p><p>Interleukin-33 (IL-33) is an IL-1 family cytokine that activates various immune cells and induces both systemic and localized Th2 responses during infection. An association between IL-33 and its suppresion of tumorigenicity 2 (ST2) receptor with inflammation during respiratory tract infection has been previously reported. Furthermore, some data suggest that during respiratory infections, IL-33 may serve as an indicator of disease severity, as high levels of this cytokine have been found in nasopharyngeal swab (NPS) samples of infants with lower respiratory tract disease caused by respiratory syncytial virus (RSV). As viral diagnosis is mostly compartmentalized in NPS, in this report, we aimed at detecting IL-33 in NPS from patients with respiratory tract infections that were collected in two different transport media (universal transport medium [UTM], and phosphate-buffered saline [PBS]). IL-33 levels were evaluated in 230 NPS samples, 121 obtained in PBS, and 109 in UTM. The samples were tested for RSV, metapneumovirus, adenovirus (ADV), influenza, and parainfluenza. In this cohort, higher levels of IL-33 were detected in virus-positive samples collected in PBS compared to virus-negative samples collected in the same transport medium. In addition, RSV- and FLU-positive samples collected in PBS showed higher measured IL-33 levels than those collected in UTM. No significant differences were found for the other viruses included in this study. These findings highlight the importance of considering sample collection and transport conditions when interpreting IL-33 measurements in NPS, particularly in future studies evaluating IL-33 as a potential severity-associated biomarker during RSV or influenza infection.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e3274290"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13579107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148977059","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":"An Optimized Feeder-Free Method for Isolation and Expansion of Functional ILC2s Isolated From Human Peripheral Blood.","authors":"Lina K Andersson, Miriam Bollmann, Agnieszka Lastowska, Isabel Haupt, Lisi Wagener, Anders Nguyen, Johan Svensson, Linda C Johansson, Mattias N D Svensson","doi":"10.1155/jimr/7688318","DOIUrl":"10.1155/jimr/7688318","url":null,"abstract":"<p><p>Innate lymphoid cells (ILCs) are tissue-resident innate counterparts of T cells. Group 2 ILCs (ILC2s) produce cytokines such as IL-5 and IL-13 in response to alarmins, including IL-25 and IL-33 and play a key role in type 2 immunity. Lately, ILC2s have become a major focus across several research areas, including asthma, allergic lung inflammation, atopic dermatitis, and liver fibrosis. However, ILC2s are rare in human peripheral blood, making their isolation and expansion for functional studies challenging. Existing methods commonly rely on flow-cytometry-based cell sorting, which requires large sample volumes, expensive reagents, and considerable hands-on time. Moreover, in vitro expansion protocols often depend on feeder cell lines and activating alarmins. Here, we present a simple and efficient approach for isolating and expanding human ILC2s from peripheral blood, without the need for flow-cytometry-based cell sorting, feeder cells, or external alarmins. This method yields pure and viable ILC2s from both large and small blood volumes, enabling the use of limited or rare patient samples. Expanded ILC2s responded robustly to alarmin stimulation by proliferating and producing signature cytokines and retained functionality after cryopreservation and reculture. Together, this method provides a user-friendly and cost-effective alternative to current human ILC2 isolation and expansion protocols.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e7688318"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13522718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840538","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":"Identification and Analysis of Biomarkers Associated With Lipid Metabolism and Ferroptosis in Ulcerative Colitis.","authors":"Xinmei Zhang, Xiufang Cui","doi":"10.1155/jimr/9283449","DOIUrl":"10.1155/jimr/9283449","url":null,"abstract":"<p><strong>Background: </strong>Mounting evidence shows that lipid metabolism and ferroptosis contribute to ulcerative colitis (UC), but the mechanism remains unclear. This study aimed to identify related biomarkers, clarify their roles in UC, and provide insights into optimized therapies.</p><p><strong>Methods: </strong>UC transcriptome, lipid metabolism, and ferroptosis-related gene (FRG) data were analyzed. Biomarkers were screened via differential expression analysis, consensus clustering, Venn, and machine learning, with expression validation. Receiver operating curve (ROC) analysis assessed predictive efficacy; functional enrichment, molecular regulatory, and immune infiltration analyses were performed. Real-time PCR verified candidate biomarkers in clinical samples.</p><p><strong>Results: </strong>Two biomarkers (acyl-CoA synthetase ligases 4 [ACSL4] and prostaglandin-endoperoxide synthase 2 [PTGS2]) were identified that distinguished UC from control samples. They may involve hematopoietic cell lines, cytokine-cytokine receptor interaction, and MALAT1 binding hsa-miR-576-5p/hsa-miR-503-5p. Notably, 27 differentially infiltrated immune cells were found (p  < 0.05), with CD56dim natural killer cells negatively correlating with ACSL4/PTGS2. Both genes were significantly upregulated in the UC clinical samples.</p><p><strong>Conclusion: </strong>ACSL4 and PTGS2 are lipid metabolism- and ferroptosis-related biomarkers of UC, laying a foundation for clinical treatment.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e9283449"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13169151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147930288","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":"Immunotherapy Resistance in dMMR/MSI-H Colorectal Cancer: Unraveling Mechanisms and Exploring Overcoming Strategies.","authors":"Ke Zhou, Ping Lu, Hongli Xu, Xinjun Liang","doi":"10.1155/jimr/5084171","DOIUrl":"10.1155/jimr/5084171","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide. Approximately 15% of localized and 5% of metastatic cases exhibit mismatch repair deficiency (dMMR) or high microsatellite instability (MSI-H). While immune checkpoint inhibitors (ICIs) have revolutionized the first-line treatment for this subgroup, 15%-46% of patients experience primary resistance, and a subset of responders eventually acquires resistance. This review synthesizes the multifaceted mechanisms underlying ICI resistance in dMMR/MSI-H CRC. We delineate tumor-intrinsic alterations, including defects in the antigen presentation machinery (specifically transporter associated with antigen processing [TAP]1/TAP2 and β₂-microglobulin [β₂m]), oncogenic signaling via the Wnt/β-catenin and JAK/STAT pathways, and epigenetic remodeling involving ARID1A. Furthermore, we explore the role of the immunosuppressive tumor microenvironment (TME), characterized by T-cell exclusion and myeloid-derived suppressor cell (MDSC) accumulation. To address these barriers, we evaluate the clinical potential of third-generation ICIs targeting lymphocyte activation gene 3 (LAG-3), T-cell immunoglobulin and mucin-domain-containing-3 (TIM-3), and TIGIT, as well as emerging biomarker strategies such as gut microbiome modulation and circulating tumor DNA (ctDNA) dynamics. By integrating these mechanistic insights with novel therapeutic approaches, including bispecific antibodies (BsAbs) and adoptive cell transfer, this review aims to provide a roadmap for overcoming resistance and advancing precision immunotherapy in dMMR/MSI-H CRC.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5084171"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13469763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148721308","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":"The Role of Neuro-Immune Regulation in the Pathogenesis of Psoriasis.","authors":"Xin Liu, Mingyu Yu, Pan Zou, Suwen Liu, Jian Jiang, Liyang Ge, Su Jiang, Jingyu Zhang, Xin Wang, Hongxiang Chen","doi":"10.1155/jimr/3016265","DOIUrl":"10.1155/jimr/3016265","url":null,"abstract":"<p><p>Psoriasis is a chronic inflammatory skin disease characterized by abnormal proliferation of epidermal cells induced by an overactive immune system. In addition to the interaction between immune cells and keratinocytes, emerging research highlights the indispensable role of peripheral sensory neurons in the initiation and progression of psoriatic inflammation. Sensory neurons not only perceive various external stimuli but also participate in skin immune regulation and barrier repair through the release of neuropeptides and neurotransmitters. This review systematically compiles current research advancements concerning the altered neural innervation patterns in psoriatic lesions, the pathophysiological functions of sensory neuron-specific receptors and ion channels, and the regulatory mechanisms of neuropeptides in disease pathogenesis. By elucidating the precise contributions of sensory neurons to the development of psoriasis, this work seeks to further clarify their specific role in the disease and provide new insights for enhancing the understanding of its pathogenesis, thereby informing the development of more targeted therapeutic strategies.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e3016265"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433400","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}