Clinical immunology最新文献

{"title":"The dual role of the COX-2/PGE2 Axis in multiple sclerosis: From pathogenesis to pharmacological inhibition","authors":"Ahmed Salem Al-Dhahi ,&nbsp;Hayder M. Al-kuraishy ,&nbsp;Nawar R. Hussain ,&nbsp;Mohamed N. Fawzy ,&nbsp;Mubarak Alruwaili ,&nbsp;Huda J. Waheed ,&nbsp;Ali I. Al-Gareeb ,&nbsp;Ali K. Albuhadily ,&nbsp;Gaber El-Saber Batiha","doi":"10.1016/j.clim.2025.110643","DOIUrl":"10.1016/j.clim.2025.110643","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is a chronic neuroinflammatory and demyelinating disease of the central nervous system (CNS). The cyclooxygenase-2/prostaglandin E2 (COX-2/PGE2) axis plays a complex, dual role in its pathogenesis. Although its upregulation typically induces neuroinflammation, oligodendrocyte apoptosis, and demyelination, certain PGE2 receptors (EP2/EP4) can also mediate protective effects. In experimental models, inhibiting COX-2 (using celecoxib or meloxicam) or blocking pro-inflammatory receptors (EP1/EP3) alleviates disease pathology by reducing immune cell infiltration and cytokine production and protecting oligodendrocytes via both COX-2-dependent and independent mechanisms. This review discusses the potential of selectively targeting the detrimental effects of the COX-2/PGE2 axis (such as EP1/EP3 signaling) while preserving protective pathways as a sophisticated therapeutic strategy for MS. However, cardiovascular risks limit the clinical translation of COX-2 inhibitors, necessitating the development of safer, more precise modulation of this pathway.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"283 ","pages":"Article 110643"},"PeriodicalIF":3.8,"publicationDate":"2025-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145594799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An integrated biomarker panel for early computational prediction of dengue severity during the acute phase","authors":"Josephine Diony Nanda ,&nbsp;Tzong-Shiann Ho ,&nbsp;Rahmat Dani Satria ,&nbsp;Yung-Ting Wang ,&nbsp;Chun-Hao Lai ,&nbsp;Ya-Lan Lin ,&nbsp;Chiou-Feng Lin","doi":"10.1016/j.clim.2025.110642","DOIUrl":"10.1016/j.clim.2025.110642","url":null,"abstract":"<div><div>Serum cytokines and chemokines play a pivotal role in dengue immunopathogenesis and may serve as biomarkers of disease severity. This study aimed to identify applicable blood biomarkers during the acute stage of infection to support early severity evaluation using Principal Component Analysis (PCA)–based feature integration. Ninety-two dengue patients were consecutively enrolled from hospital admissions with laboratory-confirmed dengue during the 2015–2017 epidemic. Only those with NS1-positive or PCR-positive cases were included in this study, spanning asymptomatic, symptomatic, and severe cases, which were assessed for hematological, viral, and cytokine/chemokine parameters. Key variables—platelet count, GPT, creatinine, NS1, NST, IL-18, RANTES, IL-6, IFN-α2, and IL-7—were incorporated into a Prediction Panel. Validation showed that several biomarker combinations achieved up to 90 % accuracy in distinguishing severity groups, while others reached ∼70 %. Principal component analysis further refined the panel, showing accuracy above 90 % when NS1 or NST were included (A–B: 92.1 %, A–C: up to 91.8 %). These findings highlight the potential of an integrated biomarker-based Prediction Panel for early and reliable assessment of dengue severity within the first week of illness.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110642"},"PeriodicalIF":3.8,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of peripheral blood mitochondrial DNA gene variation and methylation levels with rheumatoid arthritis","authors":"Qian Huang ,&nbsp;Xue-Qian Cai ,&nbsp;Zhi-Qiang Li ,&nbsp;Yan Liu ,&nbsp;Hai-Feng Pan","doi":"10.1016/j.clim.2025.110641","DOIUrl":"10.1016/j.clim.2025.110641","url":null,"abstract":"<div><h3>Objective</h3><div>Mitochondrial dysfunction is closely related to the pathogenesis of various autoimmune diseases, and mitochondrial DNA (mtDNA) gene variations are associated with the susceptibility to autoimmune diseases. This study aimed to investigate association between mtDNA genetic variants, methylation levels and rheumatoid arthritis (RA).</div></div><div><h3>Method</h3><div>We performed mtDNA whole genome sequencing in 32 RA patients and 32 controls, and then validated 8 mtDNA variants using the SNaPshot™ multiplex technique in 452 RA patients and 457 controls. The methylation levels of 4 mtDNA genes were measured in 108 RA patients and 107 controls by MethylTarget technique.</div></div><div><h3>Results</h3><div>We found that <em>ND5</em> gene m.12705 T genotype, <em>tRNA-Pro</em> gene m.16304C genotype, <em>tRNA-Pro</em> gene m.16319 A genotype were significantly associated with RA susceptibility in entire population and female population. Moreover, the increased frequency of m.12705 T and the decreased frequency of m.16304C were significantly related to anti-CCP positive in RA patients. While <em>tRNA-Pro</em> gene m.16092 T &gt; C, m.16189 T &gt; C, <em>RNR2</em> gene m.2706 T &gt; G, <em>ND2</em> gene m.4833 A &gt; G, m.5108 T &gt; C showed no association with the risk of RA. When compared to controls, the methylation levels of <em>ND5, RNR2, ND2</em> genes were significantly decreased in RA patients. In addition, <em>ND5, RNR2</em> methylation levels were linked to erythrocyte sedimentation rate, and m.12705C &gt; T variant significantly influenced <em>ND5</em> methylation level among RA patients.</div></div><div><h3>Conclusion</h3><div>Multiple mtDNA variants in <em>ND5</em>, <em>tRNA-Pro</em> genes and methylation levels of <em>ND5, RNR2, ND2</em> genes were significantly associated with genetic susceptibility to RA in Chinese population.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110641"},"PeriodicalIF":3.8,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145556372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Job's not done: BCG-itis as the first manifestation of hyper-IgE syndrome. A case report and review of the literature","authors":"Aidé Tamara Staines-Boone ,&nbsp;Edna Venegas-Montoya ,&nbsp;Jorge Alberto García Campos ,&nbsp;Jennifer Alejandra Obregón García ,&nbsp;Julieta C. Marmolejo Bjirsdorp ,&nbsp;Yuridia Salazar Gálvez ,&nbsp;Mario Ernesto Cruz-Muñoz ,&nbsp;Lizbeth Blancas Galicia ,&nbsp;Edgar Alejandro Medina-Torres ,&nbsp;Sara Elva Espinosa-Padilla ,&nbsp;Diana Olguín Calderón ,&nbsp;Laura Berrón-Ruiz ,&nbsp;Saul O. Lugo Reyes","doi":"10.1016/j.clim.2025.110639","DOIUrl":"10.1016/j.clim.2025.110639","url":null,"abstract":"<div><div>The <em>Bacille Calmette-Guérin</em> (BCG) vaccine is widely used to prevent tuberculosis (TB), especially in newborns and children in high TB prevalence areas. Though generally safe, it can cause adverse reactions like BCG-itis, a localized inflammatory response, and BCG-osis, a systemic infection. This case report details the clinical journey of a male toddler from a non-consanguineous family who presented with regional BCG-itis and later developed a disseminated mycobacterial infection. The patient had a history of recurrent suppurative otitis media and chronic granulomatous inflammation, with mycobacteria identified through biopsy. Despite initial treatments, he exhibited persistent and severe symptoms, including central nervous system abscesses, onychomycosis, and elevated serum Immunoglobulin E levels (13,160 IU/ml). Whole-exome sequencing identified a pathogenic heterozygous missense variant in <em>STAT3</em> exon 13 (c.1144C &gt; T, p.Arg382Trp), confirming autosomal dominant Hyper-IgE Syndrome. The patient showed improvement with antibiotics and intravenous immunoglobulin, yet struggled with relapses upon dose reduction of antitubercular drugs. The literature review revealed two similar cases, underscoring the importance of genetic and immunological insights in managing adverse vaccine reactions in Hyper-IgE Syndrome. CD4+ Th17 cells and interleukins 17, 21, 22, and 23 are crucial in fighting mycobacteria by activating autophagy in infected monocytes and MAIT cells. Type 2 interferon immunity and superoxide production are key in combating mycobacterial diseases like Mendelian Susceptibility to Mycobacterial Disease and Chronic Granulomatous Disease. Studies show that Asian and Latin American patients are overrepresented in non-tuberculous mycobacterial infections due to mandatory BCG vaccination at birth. It is recommended to contraindicate BCG vaccination in patients with known or suspected immune deficiencies and delay live vaccines until 6 months of age.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110639"},"PeriodicalIF":3.8,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leukemia inhibitory factor (LIF) in acute graft-versus-host disease: A hypothesis-generating review","authors":"Ahmad Meshkin ,&nbsp;Fateme Zare ,&nbsp;Mohammad Erfan Abbasi ,&nbsp;Maryam sadat Montazeri ,&nbsp;Fatemeh Badiee ,&nbsp;Mohammad Masoud Khodaei","doi":"10.1016/j.clim.2025.110640","DOIUrl":"10.1016/j.clim.2025.110640","url":null,"abstract":"<div><div>Leukemia inhibitory factor (LIF) is a multifunctional cytokine of the IL-6 family, originally identified in murine leukemia cells. Graft-versus-host disease (GvHD) is a major complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT), primarily affecting the intestine, liver, and skin. Preclinical studies suggest that LIF may protect against GvHD by preserving intestinal stem cells, reducing radiation- and cytokine-induced tissue injury, decreasing donor T-cell infiltration, and suppressing inflammatory cytokine production; importantly, it appears to preserve graft-versus-leukemia (GVL) activity. This review summarizes current knowledge on the immunopathogenesis of acute GvHD (aGvHD) and examines the emerging but limited evidence on the immunomodulatory role of LIF. We propose a hypothesis-driven framework for its potential therapeutic application. We highlight the immunomodulatory properties of LIF, including its roles in suppressing proinflammatory responses and promoting regulatory mechanisms. LIF's ability to reduce GvHD severity without compromising GVL highlights its potential as a therapeutic agent. Given the limited but promising data, further research is warranted to evaluate LIF's clinical applicability and safety in transplant recipients.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110640"},"PeriodicalIF":3.8,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IMPDH2 facilitates CD4+ T cell activation through AKT/mTOR pathway by upregulating SRPK1 in myasthenia gravis","authors":"Yingjie Ren ,&nbsp;Tao Wu ,&nbsp;Zhaojun Liu ,&nbsp;Lifang Li ,&nbsp;Ying Li ,&nbsp;Guanghao Xin ,&nbsp;Shanshan Peng ,&nbsp;Jingyan Niu ,&nbsp;Biying Chen ,&nbsp;Hanlu Cai ,&nbsp;Qinghua Tian ,&nbsp;Lihua Wang ,&nbsp;Huixue Zhang","doi":"10.1016/j.clim.2025.110634","DOIUrl":"10.1016/j.clim.2025.110634","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Myasthenia gravis (MG) is a T cell-mediated autoimmune disease characterized by abnormal immune responses, particularly the hyperactivation of CD4+ T cells, which may disrupt signal transmission at the neuromuscular junction. Inosine-5′-monophosphate dehydrogenase-2 (IMPDH2) has been reported to participate in immune activation and is likely associated with T cells, but its role in the pathogenesis of MG remains unclear. Therefore, the present study aimed to elucidate the mechanism through which IMPDH2 regulates CD4+ T cells in MG.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;In this study, IMPDH2 expression was measured by qRT-PCR in peripheral blood mononuclear cells (PBMCs) collected from 60 MG patients and 60 healthy controls. Western blotting was additionally performed to detect IMPDH2 protein expression in six MG patients (three ocular and three generalized), compared with six healthy controls matched by age, gender, and sample collection time. CD4+ T cells were then isolated from PBMCs of MG patients and healthy controls by immunomagnetic bead sorting, and IMPDH2 expression was further analyzed by qRT-PCR. Subsequently, correlations between IMPDH2 expression levels and clinical indices (neutrophil and lymphocyte counts) as well as disease severity (Myasthenia Gravis Activities of Daily Living scores and Quantitative Myasthenia Gravis scores) were assessed. Additionally, flow cytometry, EdU assays, and CCK-8 assays were employed to evaluate the effects of IMPDH2 knockdown or overexpression on CD4+ T cell apoptosis and proliferation. The expression of apoptosis-related proteins was detected by western blotting. Mass spectrometry (MS), co-immunoprecipitation (Co-IP), and kinase inhibitor-based Co-IP validation assays were used to screen and verify proteins potentially interacting with IMPDH2 in CD4+ T cells. The colocalization of IMPDH2 and its binding proteins in CD4+ T cells was confirmed by confocal fluorescence microscopy and quantitative analysis. Furthermore, western blotting was performed to assess regulatory interactions between IMPDH2 and its binding proteins upon knockdown of either molecule. Western blotting was also used to detect protein levels within MG-related signaling pathways following IMPDH2 knockdown or overexpression.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;IMPDH2 expression was significantly elevated in PBMCs and CD4+ T cells from MG patients compared with healthy controls. Clinical data analysis demonstrated a positive correlation between IMPDH2 expression and both lymphocyte and neutrophil counts in MG patients. Additionally, IMPDH2 expression positively correlated with MG disease severity. Functionally, upregulation or downregulation of IMPDH2 correspondingly promoted or suppressed CD4+ T cell proliferation and apoptosis. Mechanistically, direct interactions between IMPDH2 and SRPK1 were confirmed in vitro, and IMPDH2 was found to regulate SRPK1 expression, subsequently affecting CD4+ T cell prolifer","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110634"},"PeriodicalIF":3.8,"publicationDate":"2025-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145488124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum cytokine profiling identifies IL-17A and IL-10 as prognostic biomarkers for disease outcome in pediatric acute lymphoblastic leukemia","authors":"Qian Ye ,&nbsp;Jin Rao ,&nbsp;Li Zhang ,&nbsp;Muxia Yan ,&nbsp;Huishan Chen ,&nbsp;Yanping Yi ,&nbsp;Hua Jiang ,&nbsp;Xiaoliang Deng ,&nbsp;Yiqian Wang","doi":"10.1016/j.clim.2025.110638","DOIUrl":"10.1016/j.clim.2025.110638","url":null,"abstract":"<div><div>Pediatric acute lymphoblastic leukemia (ALL) is the most common childhood malignancy, yet reliable serum biomarkers for prognosis and relapse prediction remain limited. We profiled serum cytokines in 60 pediatric ALL patients and 19 healthy controls using the Aimplex Cytokine Assay, and evaluated predictive performance via receiver operating characteristic (ROC) analysis and least absolute shrinkage and selection operator (LASSO) regression. ALL patients exhibited significantly elevated levels of IFN-γ, IL-2, IL-4, IL-10, IL-17A, and TNF-α compared with controls. Among these, IL-17A and IL-10 showed the strongest associations with disease severity and relapse risk, with higher baseline levels correlating with increased relapse probability (<em>p</em> = 0.02 and <em>p</em> = 0.005) and longer time to achieve remission in multivariate LASSO models. These findings identify IL-17A and IL-10 as promising prognostic biomarkers for pediatric ALL, with potential application in risk stratification and guiding individualized treatment strategies.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110638"},"PeriodicalIF":3.8,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145476593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compound heterozygous NFKB1 missense variants in cis associated with immunodeficiency","authors":"Manfred Fliegauf ,&nbsp;Kelly Nitschke ,&nbsp;Pavla Mrovecova ,&nbsp;Sara Posadas-Cantera ,&nbsp;Nadezhda Camacho-Ordonez ,&nbsp;Klaus Warnatz ,&nbsp;Baerbel Keller ,&nbsp;Bodo Grimbacher","doi":"10.1016/j.clim.2025.110637","DOIUrl":"10.1016/j.clim.2025.110637","url":null,"abstract":"<div><div>Heterozygous pathogenic <em>NFKB1</em> variants are one of the most frequent monogenic causes of disease in patients with inborn errors of immunity (IEI) and mainly compromise protein expression. <em>NFKB1</em> encodes the precursor protein p105, which is processed into p50, the key transcription factor of canonical NF-κB1 signaling. Insufficiency of p105/p50 presents with immunodeficiency and autoinflammation.</div><div>Here, we evaluated two <em>NFKB1</em> missense variants, identified in compound heterozygosity <em>in cis</em> (c.[150A&gt;C;156A&gt;C]; p.[Gln50His;Lys52Asn]) in a patient with immunodeficiency. While the isomorphic Q50H variant enhanced the rather marginal defect of K52N, the combination of both caused a pathogenic protein damage in p50. Our findings highlight an inherent challenge when analyzing single variants ‘isolated’ from their genetic context. Particularly when filtering out additional variants, <em>e.g.</em> based on allele frequencies, pathogenic effects originating from compound heterozygosity may be overlooked.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110637"},"PeriodicalIF":3.8,"publicationDate":"2025-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145470831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The exacerbating role of Ras guanyl-releasing protein 1 in idiopathic inflammatory myopathies","authors":"Marina Kise ,&nbsp;Miku Shimamura ,&nbsp;Natsuka Umezawa ,&nbsp;Nao Tanaka ,&nbsp;Rihan Da ,&nbsp;Shiyao Li ,&nbsp;Tadashi Hosoya ,&nbsp;Tetsuya Saito ,&nbsp;Chikashi Terao ,&nbsp;Shinsuke Yasuda","doi":"10.1016/j.clim.2025.110636","DOIUrl":"10.1016/j.clim.2025.110636","url":null,"abstract":"<div><div>Idiopathic inflammatory myopathies (IIMs) are autoimmune disorders characterized by muscle injury mediated by both T cells and macrophages. Ras guanyl-releasing protein 1 (RasGRP1) is a guanine exchange factor for a small G protein Ras, expressed in immune cells. In this study, we investigated the role of RasGRP1 in IIMs. RasGRP1 was expressed in either CD8+, CD4+ or CD68+ cells in muscles from IIM patients as well as a murine model of myositis, C protein-induced myositis (CIM). RasGRP1 expression was upregulated in activated CD8+ T cells and macrophages <em>in vitro</em>. Response to MHC Class I-restricted stimulation in <em>Rasgrp1−/−</em> CD8+ T cells was impaired. Furthermore, <em>Rasgrp1−/−</em> mice were resistant to CIM. Differentially expressed genes between <em>Rasgrp1−/−</em> and WT mice with CIM were enriched in both adaptive and innate immune responses. These results suggested that RasGRP1 could exacerbate myositis <em>via</em> both T cells and macrophages. RasGRP1 is a possible therapeutic target for IIMs.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110636"},"PeriodicalIF":3.8,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-titer IVIG 10 % (human)–slra reduces infections and hospitalizations over 6 to 12 months: A retrospective quality improvement study","authors":"Gabrielle Magdalena Tan ,&nbsp;Kiran Sehmi ,&nbsp;Sarah Azzi ,&nbsp;Robert Hostoffer","doi":"10.1016/j.clim.2025.110633","DOIUrl":"10.1016/j.clim.2025.110633","url":null,"abstract":"<div><div>Patients with primary or secondary immunodeficiencies are at an increased risk for recurrent respiratory infections despite standard intravenous immunoglobulin (IVIG) therapy. This retrospective quality improvement review evaluated the clinical impact of a high-titer IVIG product enriched with pathogen-specific antibodies in 14 patients after failing conventional IVIG. The primary outcomes were changes in infection frequency and hospitalization rates during the 6 months before and after treatment initiation, and from 6 months post-treatment to the present. Ten patients (71%) showed clinical improvement, with infections decreasing from 36 to 8 and hospitalizations from 14 to 5 in the first 6 months post-treatment; benefits were more pronounced when excluding one clinical outlier. Two patients discontinued therapy due to mild adverse effects or lack of efficacy. High-titer IVIG was associated with meaningful reductions in infection burden and hospitalizations, supporting its consideration for high-risk patients unresponsive to standard IVIG.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110633"},"PeriodicalIF":3.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145430445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}