ImmunoTargets and Therapy最新文献

{"title":"B7-H3 (CD276) as Target for T Cell-Based Bispecific Antibody Therapy of Penile Cancer.","authors":"Aleksander Kielbik, Veronika Bahlinger, Christian M Schürch, Maria Luisa Barcena, Olesya Vakhrusheva, Anita Thomas, Igor Tsaur, Jonas S Heitmann, Helmut R Salih, Ilona Hagelstein","doi":"10.2147/ITT.S577364","DOIUrl":"https://doi.org/10.2147/ITT.S577364","url":null,"abstract":"<p><strong>Introduction: </strong>Metastatic or locally advanced penile cancer (PeCa) has limited systemic treatment options and a 5-year survival rate of ~10% in metastatic disease. Using the in vitro and ex vivo models we preclinically assessed CC-3, a B7-H3xCD3 bispecific antibody (bsAb) currently in a Phase I basket trial (NCT05999396).</p><p><strong>Methods: </strong>Primary PeCa cells were isolated from surgical specimens and characterized for surface antigen expression by flow cytometry (n = 4). B7-H3 expression was additionally evaluated in primary penile cancer tissues by immunohistochemistry (n = 10). The functional activity of the bsAb CC-3 was assessed in co-culture assays with PBMC, analyzing cytotoxicity, cytokine release, and T cell activation.</p><p><strong>Results: </strong>Immunohistochemistry of tumors from ten PeCa patients revealed strong and consistent B7-H3 (CD276) expression, with a mean H-score of 200, in tumor cells and tumor-associated vasculature, potentially enhancing T cell influx upon targeting. In vitro and ex vivo co-cultures of primary PeCa cells with peripheral blood mononuclear cells from healthy donors and PeCa patients showed that CC-3 robustly activated CD4⁺ and CD8⁺ T cells, as defined by upregulation of CD69 and CD25, with donor-dependent kinetics. CC-3 also induced potent tumor cell lysis and T cell proliferation across all patient-derived tumor samples, whereas the isotype control had no effect, confirming target-restricted activity.</p><p><strong>Discussion: </strong>These results demonstrate the strong immunostimulatory capacity of CC-3 and validate B7-H3 as a relevant target for T cell-based immunotherapy in PeCa. Our findings support the ongoing inclusion of PeCa patients in the clinical CC-3 trial and encourage further development of B7-H3-directed strategies for this rare, understudied malignancy.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"577364"},"PeriodicalIF":4.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13142290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843597","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":"Tumor-Promoting Crosstalk of MMP11⁺ Fibroblasts and SPP1⁺ Macrophages Drive Poor Prognosis in Breast Cancer: Integrated Multi-Omics Analysis.","authors":"Rongzhi Huang, Zexu Zhan, Shulin Huang, Wenlong Cao, Jiehua Li, Min Mao","doi":"10.2147/ITT.S564498","DOIUrl":"https://doi.org/10.2147/ITT.S564498","url":null,"abstract":"<p><strong>Introduction: </strong>Breast cancer (BRCA) remains the leading cause of cancer-related mortality among women and poses significant therapeutic challenges. While the heterogeneity of the tumor microenvironment (TME) is well established as a key contributor to tumor progression and treatment failure, yet the specific stromal-immune interactions driving these processes remain poorly understood.</p><p><strong>Methods: </strong>We employed an integrated multi-omics approach, combining bulk RNA sequencing, single-cell RNA sequencing, and spatial transcriptomics, to systematically characterize the cellular landscape of the BRCA TME.</p><p><strong>Results: </strong>Our analysis revealed a distinct population of MMP11⁺ cancer-associated fibroblasts (CAFs). MMP11⁺ CAFs were significantly enriched in BRCA tissues and were associated with unfavorable prognosis. Functional analysis revealed that MMP11⁺ CAFs were associated with tumor progression by enhancing angiogenesis and epithelial-mesenchymal transition (EMT). Moreover, our study uncovered that a significant interaction between MMP11⁺ CAFs and SPP1⁺ macrophages that was strongly associated with poor outcomes. Patients with high MMP11⁺ CAFs and SPP1⁺ macrophages were associated with adverse overall survival and might impaired immunotherapy response.</p><p><strong>Conclusion: </strong>Our study identifies a distinct population of MMP11⁺ CAFs that is highly enriched in BRCA. We further elucidated a close interaction between MMP11⁺ CAFs and SPP1⁺ macrophages within the BRCA tumor microenvironment. Targeting this stromal-immune interaction represents a promising therapeutic target for future BRCA treatment strategies.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"564498"},"PeriodicalIF":4.4,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843616","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":"RNA Sequencing Analyses and Validation of Immune-Related Genes in EBV-Specific Cytotoxic T Lymphocytes During Latent Infection.","authors":"Zhen Guan, Xiulan Ao, Lili Zhou, Chunhong Yu, Zhiqiang Zhang, Dongliang Li","doi":"10.2147/ITT.S568661","DOIUrl":"https://doi.org/10.2147/ITT.S568661","url":null,"abstract":"<p><strong>Background: </strong>Epstein-Barr virus (EBV) infects more than 90% of the global population, but the immune mechanism underlying its infection remains incompletely understood.</p><p><strong>Methods: </strong>In this study, transcriptomic profiling and validation of differentially expressed genes (DEGs) were performed between Epstein-Barr virus-specific cytotoxic T lymphocytes (EBV-CTLs) and nonspecific CTLs via RNA sequencing (RNA-seq). Bioinformatics analyses, including Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, functional molecular module construction, and key gene analysis, were conducted to explore the biological functions and potential regulatory mechanisms of the DEGs.</p><p><strong>Results: </strong>A total of 1236 DEGs were identified in the EBV-CTL group compared with the nonspecific CTL group, including 645 upregulated genes and 591 downregulated genes. GO enrichment analysis revealed that these DEGs were localized mainly to cell membranes and MHC class II protein complexes and were involved in biological processes such as cellular defense, leukocyte activation, proliferation, differentiation, and chemotaxis. KEGG pathway enrichment analysis revealed that the JNK/p38 MAPK pathway was the most significantly enriched signaling pathway, with key DEGs including <i>p38, HSP72</i>, and components of the AP-1 transcription factor complex (mainly <i>JUN</i> and <i>FOS</i>). The functional molecular module construction revealed that the top-scoring modules were associated primarily with signal transduction, the inflammatory response, the immune response, and molecular interactions (eg, protein and receptor binding). Key gene analysis identified <i>JUN, FOS, TNF</i>, and <i>STAT1</i> as potential hub genes involved in the EBV-specific immune response.</p><p><strong>Conclusion: </strong>Our transcriptomic analysis reveals the unique gene expression profile of EBV-CTLs and identifies the JNK/p38 MAPK pathway and hub genes (<i>JUN, FOS, TNF, and STAT1</i>) as critical regulators of the EBV-specific immune response. These findings provide novel insights into the molecular mechanism underlying EBV-specific immunity and potential targets for related therapeutic intervention.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"568661"},"PeriodicalIF":4.4,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147821646","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":"Blinatumomab for Pediatric High-Risk B-Cell Precursor Acute Lymphoblastic Leukemia: Safety, MRD Response and Survival in a Single-Center Retrospective Cohort.","authors":"Małgorzata Mitura-Lesiuk, Patrycja Najda, Oliwia Rdzanek, Julia Bogucka, Karolina Różycka, Maciej Dubaj, Joanna Zawitkowska","doi":"10.2147/ITT.S603087","DOIUrl":"https://doi.org/10.2147/ITT.S603087","url":null,"abstract":"<p><strong>Background: </strong>Advances in the treatment of pediatric acute lymphoblastic leukemia (ALL) have significantly improved outcomes, with overall survival rates exceeding 90%. Despite these favorable results, relapse and resistance to therapy remain major clinical challenges, and ALL is still the second leading cause of cancer-related mortality in children, after central nervous system tumors. The development of immunotherapy has led to new treatment options, including blinatumomab. The aim of this study was to assess the efficacy of blinatumomab treatment and to evaluate its safety profile in pediatric patients with high-risk precursor B-cell ALL.</p><p><strong>Material and methods: </strong>We conducted a retrospective single-center cohort study including 13 pediatric patients with high-risk BCP-ALL treated with blinatumomab between 2017 and 2025 in Lublin, Poland. Primary outcomes were MRD negativity and overall survival. Safety was assessed using CTCAE criteria.</p><p><strong>Results: </strong>MRD positivity before treatment was present in 8/13 patients. After the first cycle, 62.5% achieved MRD negativity, increasing to 75.0% overall after two cycles. Kaplan-Meier estimated 12-month OS was 83.3%, and 24-month OS was 64.8%. Adverse events occurred in 69.2% of patients; grade 3 toxicity in 23.1%. No life-threatening toxicity occurred.</p><p><strong>Conclusions: </strong>In this small retrospective cohort, blinatumomab demonstrated encouraging MRD response, favorable survival estimates, and acceptable tolerability in pediatric high-risk BCP-ALL. Larger prospective multicenter studies are warranted.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"603087"},"PeriodicalIF":4.4,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13117821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783338","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":"New Insights on IgA Nephropathy from the Perspective of Active Lesions and Systemic Inflammatory Responses.","authors":"Yang Yang, Gaosi Xu","doi":"10.2147/ITT.S585437","DOIUrl":"https://doi.org/10.2147/ITT.S585437","url":null,"abstract":"<p><p>Immunoglobulin A nephropathy (IgAN) is a chronic disease. Active disease typically presents with massive proteinuria and gross hematuria, along with renal pathological features such as mesangial cell proliferation, endothelial cell proliferation, and crescents. Active lesions may achieve remission following treatment but also can relapse at any stage of the patient's life. Systemic inflammatory markers are significantly associated with IgAN disease activity indicators. Research has found that patients with high disease activity and low chronicity are more likely to benefit from immunosuppressive therapy. We speculated that \"four-hit\" hypothesis in IgAN may exist as the background for the recurrence of the disease. Bacterial or viral infections and vaccinations are common mucosal triggers that may induce active lesions by activating systemic inflammatory responses. The clinical manifestations triggered by these factors are diverse, which likely reflects the complex interplay between the nature of the injury and individual patient susceptibility. In this narrative review, we explore new insight on IgAN from the perspective of active disease and systemic inflammatory responses.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"585437"},"PeriodicalIF":4.4,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783295","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":"Multi-Omics Analysis Reveals m7G Methylation-Related Genes May Be Involved in TGF-β Signaling-Mediated Anti-PD-L1 Response in Bladder Cancer.","authors":"Hai-Qi Liang, Yu-Jian Li, Jia-Yin Yu, Qi-Zhou Mo, Qiu-Ju Wei, Yu-Qi Liang, Fa-Ye Wei, Xiao-Ping Zhang, Jia-Wen Zhao, Yu-Xian He, Xin-Dong Feng, Bin-Tong Yin, Xin-Wen Liang, Ren-Jun Nong, Yao-Yu Wang, Min Qin, Ji-Wen Cheng","doi":"10.2147/ITT.S583577","DOIUrl":"https://doi.org/10.2147/ITT.S583577","url":null,"abstract":"<p><strong>Background: </strong>Immunotherapy resistance is a significant challenge in bladder cancer treatment. The role of N7-methylguanosine (m7G) methylation in this process remains unclear. This study aims to investigate the potential role of m7G methylation-related genes (m7GRGs) in immunotherapy resistance using a multi-omics approach.</p><p><strong>Methods: </strong>This study integrated bioinformatics analysis with in vitro experimental validation. We obtained bulk, single-cell, and spatial transcriptomics data from multiple bladder cancer cohorts in public databases, including TCGA, GEO and IMvigor210. Machine learning models were performed to identify molecular clusters and screen signature genes. Gene ontology analysis was used for gene function enrichment. siRNA transfection knocked down the expression of characteristic genes in bladder cancer cell lines to validate their roles in signaling regulation. Gene expression was assessed using qRT-PCR, Western blot, and immunohistochemistry. Additionally, CCK-8 and wound healing assays were performed to evaluate the effects of characteristic genes on the proliferation and migration of bladder cancer cells.</p><p><strong>Results: </strong>Two bladder cancer molecular clusters were identified, with the C1 cluster exhibiting worse prognosis, higher m7GRGs expression, and an immunosuppressive microenvironment. NUDT10 was a key prognostic gene distinguishing molecular clusters. A subset of differentially methylated genes correlated with anti-PD-L1 resistance were enriched in the TGF-β signaling pathway. Single-cell and spatial transcriptomics revealed that NUDT10 was co-expressed with TGF-β activator LRRC32. IMvigor210 and GSE176307 datasets found that expression of NUDT10 and LRRC32 was associated with poor response to anti-PD-L1 therapy. Knockdown of NUDT10 in bladder cancer cells inhibited the expression of LRRC32 and reduced the proliferation and migration abilities of the cancer cells.</p><p><strong>Conclusion: </strong>This study identifies NUDT10 as a key gene associated with poor prognosis based on m7GRGs-defined molecular clusters in bladder cancer. NUDT10 expression may regulate TGF-β signaling and is associated with poor response to anti-PD-L1 therapy in advanced or metastatic bladder cancer.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"583577"},"PeriodicalIF":4.4,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13092455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147783322","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":"Cryoablation Plus Immune Checkpoint Inhibitors Enhanced Dendritic Cell and T Cell Activation in TNBC Murine Model.","authors":"Flavia Sardela de Miranda, Rachel L Babcock, Maria F Mahecha, Prrishti J Gukhool, Geetha P Boligala, Amanda K Garcia, Dalia Martinez-Marin, Ava G Oliver, Thomas Hintelmann, Kathryn L Furr, Chhanda Bose, Sharilyn Almodovar, Sharda P Singh, Kevin Pruitt, Michael W Melkus, Rakhshanda Layeequr Rahman","doi":"10.2147/ITT.S581990","DOIUrl":"https://doi.org/10.2147/ITT.S581990","url":null,"abstract":"<p><strong>Purpose: </strong>Cryoablation eradicates tumors through repeated freeze-thaw cycles and preserves tumor-associated antigens, triggering inflammatory signals capable of priming anti-tumor immunity, yet its therapeutic potential in triple-negative breast cancer (TNBC) remains largely unexplored. Immune checkpoint inhibitors (ICIs) have shown clinical benefit in TNBC but come with significant immune-related toxicities. Combining cryoablation with ICIs in TNBC may amplify the efficacy of cryoablation, which is significantly less toxic than ICIs, thereby providing opportunities for lowering the doses of ICIs in clinical practice. Here, we investigated the therapeutic impact of cryoablation with ICIs in an orthotopic bilateral murine TNBC model.</p><p><strong>Methods: </strong>Two weeks after tumor induction, primary tumors were cryoablated while the abscopal tumors were not manipulated and represented distant tumors. Twenty-four hours pre- and post-cryoablation, mice received an intra-peritoneal injection of PBS or ICIs (anti-CTLA-4, PD-1, or PD-L1). Tumors, tumor-draining lymph nodes (TdLNs), spleen, and peripheral blood were assessed for immune profiling a week later.</p><p><strong>Results: </strong>Preliminary analyses demonstrated that combining cryoablation with anti-CTLA-4 enhanced T cell activation systemically compared to cryoablation alone or in combination with PD-1/PD-L1 blockade. Notably, relative to cryoablation monotherapy, combination with anti-CTLA-4 increased the frequencies of activated CD4⁺ and CD8⁺ T cells in the abscopal tumors, while also inducing a higher frequency and activation of conventional dendritic cells in the abscopal TdLNs.</p><p><strong>Conclusion: </strong>These results suggest combination of cryoablation with anti-CTLA-4 therapy enhances systemic antitumor immunity by boosting antigen presentation. Our results support further investigation into this combination strategy to prevent tumor recurrence and metastasis while minimizing toxicity of treatment.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"581990"},"PeriodicalIF":4.4,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13070197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147676641","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":"Guillain-Barré Syndrome: Progress in Diagnosis, Biomarkers, Neuroimaging and Management.","authors":"Joumana Freiha, Young Gi Min, Chinar Osman, Yusuf A Rajabally","doi":"10.2147/ITT.S390161","DOIUrl":"https://doi.org/10.2147/ITT.S390161","url":null,"abstract":"<p><p>Guillain-Barré syndrome (GBS) is the leading cause of acute flaccid paralysis worldwide and represents a heterogenous spectrum of acute autoimmune polyradiculoneuropathies. Over the past decade, large international cohorts and advances in neuroimmunology have improved understanding of its clinical subtypes, infectious triggers, and pathophysiology. This review summarises recent progress across key aspects of diagnosis, prognostication, and treatment. We first describe updated perspectives of clinical heterogeneity including GBS variants and geographical variability, and the recognition of autoimmune nodopathies as an important differential diagnosis. We then discuss updated knowledge on antecedent infections including <i>Campylobacter jejuni</i> and anti-ganglioside antibodies, as well as the revised role of electrodiagnosis, as an exclusively diagnostic tool rather than allowing definite and meaningful subtype classification. Established prognostication models such as Erasmus GBS Outcome Score and Erasmus GBS Respiratory Insufficiency Score as well as emerging fluid biomarker candidates spanning biochemical, immunological, nerve-structural markers are reviewed. Advances in neuroimaging that aid in diagnosis and subtyping of GBS are also discussed. Finally, we highlight the evidence reaffirming intravenous immunoglobulin or plasma exchange as current standard-of-care and critically evaluate ongoing and recently completed trials including complement inhibitors.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"390161"},"PeriodicalIF":4.4,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13052254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634514","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":"Circulating miR-148a-3p Correlates with Inadequate Induction Response in Pediatric Hodgkin Lymphoma.","authors":"Marius Rohde, Vijay Kumar Singh, Andrea Wolfermann, Birgit Burkhardt, Claudia Blattmann, Daniel Steinbach, Dominik T Schneider, Martin Ebinger, Britta Maecker-Kolhoff, Matthias Braun, Lars Kurch, Christine Mauz-Körholz, Dieter Körholz","doi":"10.2147/ITT.S577426","DOIUrl":"https://doi.org/10.2147/ITT.S577426","url":null,"abstract":"<p><p>Pediatric Hodgkin lymphoma (HL) is highly curable, and reducing the treatment intensity in patients who respond well to induction therapy is a key strategy for minimizing long-term adverse effects. Biomarkers that identify good responders at diagnosis would enable further de-escalation of the treatment. Circulating microRNAs (miRNAs) have shown promise as noninvasive indicators of therapeutic response in hematological cancers, yet their association with early metabolic response on quantitative 18F-Fluorodeoxyglucose-Positron Emission Tomography (18F-FDG-PET) in pediatric HL has not been defined. Here, we investigated the potential of circulating miRNAs to predict the response to induction therapy in pediatric HL. Small RNA sequencing of serum samples from 35 patients revealed 24 Hodgkin lymphoma-associated miRNAs that were differentially expressed between adequate and inadequate responders. Subsequent quantitative reverse transcription-polymerase chain reaction (qRT-PCR) validation demonstrated significantly elevated miR‑148a‑3p levels at diagnosis in inadequate responders to induction therapy than in adequate responders (p=0.009). These results indicate that circulating miR‑148a‑3p may enhance current predictive approaches by identifying high‑risk patients less likely to achieve rapid metabolic remission.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"577426"},"PeriodicalIF":4.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13050980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634503","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":"Comparative Clinical and Electrophysiological Profiles of Chronic Inflammatory Demyelinating Polyneuropathy in Patients with and without Diabetes Mellitus: An Observational Study.","authors":"Abdullah Al Mamun, Most Samsun Nahar Sumi, Mohammad Enayet Hussain, A F M Al Masum Khan, Mohammad Aftab Rassel, Ghulam Kawnayn, Md Abdullah Yusuf, Redoy Ranjan, Adneen Moureen, Dipannita Adhikary, Md Badrul Alam, Quazi Deen Mohammad, Md Nazmul Karim","doi":"10.2147/ITT.S592658","DOIUrl":"10.2147/ITT.S592658","url":null,"abstract":"<p><strong>Background: </strong>Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an immune-mediated, treatable neuropathy with clinical and electrophysiological features that overlap with diabetic polyneuropathy, complicating diagnosis and delaying immunotherapy. This study compared the clinical and electrophysiological characteristics of CIDP in patients with and without diabetes mellitus (DM) to determine whether diabetes modifies disease presentation or severity.</p><p><strong>Methods: </strong>This cross-sectional comparative study was conducted at the National Institute of Neurosciences and Hospital, Dhaka, Bangladesh, from January 2018 to December 2023. Consecutive patients aged ≥15 years with CIDP diagnosed per EFNS/PNS 2010 criteria and reclassified using 2021 EAN/PNS guidelines were enrolled and stratified into CIDP+DM and CIDP-DM groups. Clinical data, disability scores (MRCSS, I-RODS, INCAT), and electrophysiological parameters were compared using Mann-Whitney U and chi-square tests.</p><p><strong>Results: </strong>Of 143 patients (21 CIDP+DM; 122 CIDP-DM), those with diabetes were older at symptom onset (median 55 vs 45 years, p = 0.034) and demonstrated significantly greater distal muscle weakness (p = 0.045), though overall disability scores were comparable. Electrophysiological assessment confirmed demyelination in both groups; however, CIDP+DM patients exhibited more pronounced axonal involvement, evidenced by reduced median and ulnar compound muscle action potential amplitudes (p = 0.034-0.046) and increased tibial F-wave abnormalities (p = 0.042). In age- and sex-adjusted multivariable analyses, diabetes independently modified CIDP by reducing distal muscle power (β = -1.13; p < 0.001), median CMAP at elbow (β = -1.32 mV; p = 0.0006), ulnar CMAP at wrist (β = -1.97 mV; p = 0.0004) and elbow (β = -1.55 mV; p < 0.001), tibial F-wave presence (β = -0.46; p = 0.0002), and overall function with lower MRCSS (β = -3.20; p = 0.04) and higher INCAT scores (β = 1.81; p = 0.004).</p><p><strong>Conclusion: </strong>Diabetes modifies CIDP, producing a mixed demyelinating-axonal phenotype with greater distal motor impairment.</p>","PeriodicalId":30986,"journal":{"name":"ImmunoTargets and Therapy","volume":"15 ","pages":"592658"},"PeriodicalIF":4.4,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147594958","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}