Journal of Immunology Research最新文献

{"title":"Epigenetic Modulation of IL-7 and IL-10: Toward Personalized Immune Therapies in Viral Epidemics.","authors":"Zerrin Yulugkural, Mustafa Yildiz, Ertugrul Topcu, Habibe Tülin Elmaslar Mert, Alp Temiz","doi":"10.1155/jimr/9467657","DOIUrl":"10.1155/jimr/9467657","url":null,"abstract":"<p><strong>Background: </strong>Host immune responses, including cytokine production, shape the severity of viral epidemics. Epigenetic mechanisms such as DNA methylation regulate cytokine gene expression and may contribute to immune dysregulation in severe disease.</p><p><strong>Methods: </strong>This study analyzed interleukin-7 (IL-7), IL-8, and IL-10 promoter methylation in 145 COVID-19 patients (91 wards, 54 intensive care units (ICUs)), excluding 12 patients receiving epigenetically active drugs. Peripheral blood DNA underwent bisulfite conversion, followed by PCR and gel electrophoresis. Gene-specific methylation levels were quantified using beta values.</p><p><strong>Results: </strong>IL-7 was significantly hypermethylated overall (β = 0.835, <i>p</i> < 0.001), especially in ICU patients (β = 0.863, <i>p</i> = 0.001), independent of age, mortality, and malignancy. An interaction between age and ICU status indicated group-specific effects. IL-10 showed significant hypomethylation (β = 0.243, <i>p</i> < 0.001), while IL-8 methylation did not differ significantly (<i>p</i> = 0.373). ICU patients had higher mortality (26% vs 5.5%, <i>p</i> < 0.001).</p><p><strong>Conclusion: </strong>IL-7 hypermethylation may impair T-cell-mediated immunity in severe cases, while IL-10 hypomethylation may reflect enhanced immunosuppression. These findings suggest a role for epigenetic cytokine regulation in disease progression and may guide future immunomodulatory strategies.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 ","pages":"9467657"},"PeriodicalIF":3.2,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12780970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145952034","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":"Neutrophil Plasticity and NETosis in Tumour Microenvironment: Tumour Evolution and Therapy Resistance.","authors":"Mojdeh Soltani, Sara Falahi, Mohammad Abbaszadeh, Mark J M Sullman, Hamed Fouladseresht, Nahid Eskandari","doi":"10.1155/jimr/5568021","DOIUrl":"10.1155/jimr/5568021","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs) are web-like formations consisting of DNA-histone complexes and associated proteins released from activated neutrophils. While NET formation plays an important role in innate immunity, it is also associated with the pathogenesis of autoimmune disorders such as rheumatoid arthritis, psoriasis and systemic lupus erythematosus. Research suggests that NETosis (the process of NET formation) may contribute to the progression of cancer and the spread of malignant tumours. A clear link exists between the accumulation of neutrophils in the tumour microenvironment (TME), known as tumour-associated neutrophils (TANs) and NETosis activation in both primary and metastatic tumours. Furthermore, the literature highlights the role of NETs in modulating immune surveillance within the TME. This review aims to analyse the interplay between NETosis and the TME, emphasising its implications for tumour progression, immune evasion and resistance to therapy.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 ","pages":"5568021"},"PeriodicalIF":3.2,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12771616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917615","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":"High Concentrations of β₂-Microglobulin Do Not Inhibit In Vitro Generation of Functional Dendritic Cells.","authors":"Pavla Taborska, Dmitry Stakheev, Katerina Krausova, Jirina Bartunkova, Daniel Smrz","doi":"10.1155/jimr/2924555","DOIUrl":"10.1155/jimr/2924555","url":null,"abstract":"<p><p>β₂-microglobulin (β2M) is a small protein playing a critical role in stabilizing major histocompatibility complex class I (MHC-I) molecules on nucleated cells. Elevated levels of β2M have been observed in several cancers, inflammatory and autoimmune conditions, and renal failures. High concentrations of β2M were reported to inhibit in vitro generation of functional dendritic cells (DCs). However, our findings showed that β2M exerts a negative effect on DCs only when contaminated with endotoxins. We found that β2M preparations with a high level of endotoxin impurities matured DCs, but that this effect was not seen with functional β2M preparations with low levels of endotoxin impurities, thus showing the maturation effect was due to endotoxin stimulation. We confirmed that the high-level endotoxin β2M compromised the in vitro differentiation of monocytes into DCs. In contrast, a low-level endotoxin β2M had no negative impact on DC differentiation nor prevented their maturation and functionality. Moreover, regardless of the levels of endotoxin impurities, β2M stabilized the expression of MHC-I molecules, confirming its functionality in the experimental settings. Our results show that β2M does not compromise the differentiation of DCs and indicate that elevated levels of β2M are unlikely to negatively regulate the immune system. These results have significant implications for understanding the functions of high β2M concentrations in clinical contexts and in vitro applications.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 ","pages":"2924555"},"PeriodicalIF":3.2,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12771628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917596","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 Exploratory Study of the Impact of a CCL21-Derived C-Terminal Peptide on Dendritic Cell Lymph Node Homing.","authors":"Marina Barrio-Calvo, Astrid Sissel Muldorff Frellsen, Emma Probst Brandum, Mette Marie Rosenkilde, Eoghan Connors, Per Basse, Pawel Kalinski, Gertrud Malene Hjortø","doi":"10.1155/jimr/8833079","DOIUrl":"10.1155/jimr/8833079","url":null,"abstract":"<p><p>The effective trafficking of dendritic cells (DCs) to the lymph nodes (LNs), orchestrated by CC-chemokine receptor 7 (CCR7) and its ligand CCL21, is essential for the success of DC-based immunotherapies. This study explores the potential of C21TP, a naturally occurring basic peptide derived from the C-terminal of CCL21, to enhance DC homing to the draining LNs in a murine model of DC migration. C21TP, containing three clusters of basic residues, significantly boosts CCL21-mediated signaling and chemotaxis of DCs in vitro. In vivo, DCs formulated with C21TP prior to injection migrated more efficiently to the draining LNs than DCs alone or DCs formulated with a mutated version of C21TP, harboring substitutions in key basic residues. Further studies are needed to evaluate the impact of C21TP on T-cell priming efficacy in the context of DC-based immunotherapies. Nonetheless, C21TP's ability to enhance lymph node homing of adoptively transferred cells without additional cellular modifications could offer a practical and scalable approach for advancing future DC-based vaccines.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 ","pages":"8833079"},"PeriodicalIF":3.2,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12771625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917573","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":"Myeloid-Derived Suppressor Cells (MDSCs) Suppress T-Cell Proliferation Less Than Mature Neutrophils in Blood and Bone Marrow From Multiple Myeloma Patients.","authors":"Julia Westerlund, Sandra Askman, Åsa Pettersson, Stina Wichert, Thomas Hellmark, Åsa C M Johansson, Markus Hansson","doi":"10.1155/jimr/9232540","DOIUrl":"10.1155/jimr/9232540","url":null,"abstract":"<p><p>Multiple myeloma (MM) is the second most common hematological malignancy, characterized by a clonal expansion of malignant plasma cells in bone marrow. Monoclonal gammopathy of undetermined significance (MGUS) is the premalignant condition of MM. The tumor microenvironment is thought to influence the progression from premalignant conditions. Myeloid-derived suppressor cells (MDSCs) are a heterogenous group of different cellular subsets with myeloid origin, characterized by their ability to inhibit T-cell responses. MDSC are thought to play an important immunoregulatory role in different diseases, and in many cancers their levels seem to correlate with a poor prognosis. There are three different subsets, the neutrophil-like polymorphonuclear (PMN)-MDSC, the monocyte-like (M)-MDSC, and the immature early (e)MDSC. In this study, we investigate the levels and functions of all MDSC subsets in the bone marrow of both MGUS and MM patients and compare it to blood MDSC. We found that MDSC levels are not increased in neither the blood nor bone marrow of MGUS or MM patients, and they lack strong T-cell suppressive abilities. Blood PMN-MDSC seems to have a small inhibitory effect, but mature neutrophils were more suppressive. Interestingly, eMDSC levels were decreased in the blood of MM patients. Our data indicate that MDSC are not key players in the pathogenesis of MM, but that mature neutrophils may be more important as they have a stronger immunoregulatory effect.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 ","pages":"9232540"},"PeriodicalIF":3.2,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12771638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917568","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":"Resolving the Interference of Anti-CD38 Antibodies on Blood Compatibility Assays Using CD38 \"Baitbodies\" Approach.","authors":"Dianne Celine Gnann, Stephan Steinke, Hendrikus S P Garritsen, Michael Hust","doi":"10.1155/jimr/7343647","DOIUrl":"10.1155/jimr/7343647","url":null,"abstract":"<p><p>Blood transfusion safety depends on swift blood compatibility testing. Alloantibodies recognizing these blood group antigens determine blood compatibility, and the transfusion of incompatible blood can lead to life-threatening hemolytic transfusion reactions. Recently, the landscape of blood compatibility testing has been complicated due to the interference caused by therapeutic antibodies targeting CD38, a key target in cancer immunotherapy that is also expressed on red blood cells. The presence of anti-CD38 antibodies in blood samples has been found to bind to test or donor red blood cells, resulting in false positive tests. This interference poses a serious risk as it can potentially mask immunogenic alloantibodies and cause delays in supplying safe blood products. We present the development and application of fragment crystallizable (Fc)-fusion constructs, referred to as \"baitbodies\", designed to neutralize anti-CD38 antibodies and mitigate false positive test outcomes. The extracellular domain of CD38 was fused to the Fc domain of a murine immunoglobulin G. These baitbody constructs were thoroughly characterized and applied in both serological microcolumn agglutination and automated solid-phase red cell adherence assays. The CD38-mFc baitbody successfully prevented agglutination reactions induced by three clinically relevant anti-CD38 monoclonal antibodies-daratumumab, felzartamab and isatuximab-in spiked samples. This allowed the detection of alloantibodies of the Rhesus, Kell and Duffy blood groups without interference. The CD38-mFc construct also demonstrated potential in a head-to-head comparison with commercial mitigation reagents, DaraEx and Grifols sCD38. Finally, the CD38-mFc baitbody effectively neutralized daratumumab in patient samples, preventing false positive test outcomes.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 ","pages":"7343647"},"PeriodicalIF":3.2,"publicationDate":"2026-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12765988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911983","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":"Immune System and Hepatic Stellate Cells' Crosstalk in Liver Fibrosis: Pathways and Therapeutic Potential.","authors":"Wahyu Widowati, Adilah Hafizha Nur Sabrina, Annisa Firdaus Sutendi, Fadhilah Haifa Zahiroh, Aris Muhamad Nurjamil, Teresa Liliana Wargasetia, Ita Margaretha Nainggolan, Rizal Azis, Elham Rismani, Massoud Vosough","doi":"10.1155/jimr/2656395","DOIUrl":"10.1155/jimr/2656395","url":null,"abstract":"<p><p>Liver fibrosis, characterized by the excessive deposition of extracellular matrix (ECM) driven by hepatic stellate cells (HSCs) activation, remains a critical challenge due to its progression to cirrhosis and hepatocellular carcinoma (HCC). This review clarifies the complex crosstalk between the immune system and HSCs, highlighting key cellular players including macrophages, natural killer (NK) cells, regulatory T cells (Tregs), and their cytokine-mediated signaling pathways that regulate fibrogenesis and fibrosis resolution. We describe pivotal molecular mechanisms such as transforming growth factor (TGF)-β, platelet-derived growth factor (PDGF), Wnt/β-catenin, and NF-κB signaling in HSCs modulation, emphasizing their interplay with immune responses. Novel therapeutic strategies targeting this complex immune-HSCs interaction, ranging from immunomodulatory agents, macrophage polarization, and NK cell-based therapies, to stem cell-derived exosomes, offer promising opportunities for preventing and reversing fibrosis. We further discuss innovative combination therapies integrating immunotherapies with antifibrotic agents, personalized strategies based on immune profiling, and the challenges of immune heterogeneity in fibrosis management. This review discusses recent advances in molecular interplay of immune system and HSCs, highlighting novel therapeutic targets, and future perspectives for managing chronic liver diseases.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 ","pages":"2656395"},"PeriodicalIF":3.2,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12759114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145900559","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":"Analysis of the Mediating Effect of Vitamin D via the TGF-β1/Treg Pathway in the Pathogenesis of Childhood Primary Immune Thrombocytopenia.","authors":"Peiling Li, Mengru Chen, Zhihang Wang, Rui Fan, Jia Guo, Bao Liu, Zhiyin Wang, Yanyan Ma, Dongju Zhao, Shujun Li","doi":"10.1155/jimr/4001873","DOIUrl":"10.1155/jimr/4001873","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of vitamin D (VitD), transforming growth factor-β1 (TGF-β1), and regulatory T cells (Treg) in the pathogenesis of primary immune thrombocytopenia (ITP) in children.</p><p><strong>Methods: </strong>From February 2023 to September 2024, 51 children with ITP and 44 healthy children from the First Affiliated Hospital of Xinxiang Medical College were enrolled. The serum levels of VitD and TGF-β1 and the percentage of Treg cells in peripheral blood were measured.</p><p><strong>Results: </strong>There was no significant difference in age and sex between the two groups (p  > 0.05). ITP group VitD, TGF-β1, and the level of Treg cells were significantly lower than those of the control group (p  < 0.05). In the ITP group, VitD and TGF-β1 (r = 0.421), Treg cells (r = 0.516), TGF-β1 and Treg cells (r = 0.563), and platelet count (r = 0.399, 0.305, 0.361, respectively, p  < 0.05). The median model analysis showed that VitD had a significant negative overall effect on ITP risk (regression coefficient = -0.014, p = 0.004), but its direct effect was no longer significant after the introduction of TGF-β1 and Treg, suggesting a complete mediation effect, where the path of VitD affecting ITP via TGF-β1 is significant (effect value = -0.015, p  < 0.001), but the mediated pathway involving Treg was not statistically significant.</p><p><strong>Conclusion: </strong>There is dysregulation of VitD, TGF-β1, and Treg cells in newly diagnosed children with ITP. TGF-β1 may be a key mediator of the regulation of ITP by VitD, suggesting the potential value of TGF- β1 as an intervening target.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e4001873"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512629","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":"CD47 Expression in Classic Hodgkin Lymphoma and Its Association With Tumor Microenvironment.","authors":"Xiaoyue Xiao, Lin Nong, Yiyang Luo, Jiyan Dong, Xujie Sun, Kang Jiang, Xuemin Xue, Xiaoli Feng","doi":"10.1155/jimr/1680256","DOIUrl":"10.1155/jimr/1680256","url":null,"abstract":"<p><p>Cluster of differentiation 47 (CD47) has been reported to overexpress in various malignant tumors and is associated with inferior prognosis. However, the critical role of CD47 in classic Hodgkin lymphoma (CHL) and its association with immune checkpoints and tumor microenvironment (TME) remain unclear. Tumor tissues of CHL from Cancer Hospital, Chinese Academy of Medical Sciences and the public dataset from GSE17920 were analyzed. Immunohistochemistry was performed to detect the expression of CD47, programmed cell death protein 1 (PD-1), and PD ligand 1 (PD-L1) in CHL. Kaplan-Meier curves and Cox model were used for comparing the clinical outcomes of patients belonging to different subgroups. Bioinformatic analyses included differentially expressed genes (DEGs) screening, functional enrichment, and immune infiltration (CIBERSORT) were performed using GSE17920. In the study, CD47 expression was analyzed in both tumor cells (CD47tumor_score) and the TME (CD47micro_score) of CHL patients. High CD47tumor_score was associated with poorer progression-free survival (PFS) (p = 0.04). Meanwhile, high CD47micro_score was significantly correlated with worse PFS (p = 0.02). Univariate Cox regression identified high CD47micro_score as a significant predictor of inferior overall survival (OS; hazard ratio [HR] = 4.91, p = 0.03). Additionally, high CD47 expression correlated with increased PD-L1, and patients with concurrent high CD47 and positive PD-L1 of tumor cells had the shortest PFS, although this trend was not statistically significant. Importantly, a synergistic prognostic effect between CD47 and PD-L1 was that patients with high CD47 and/or PD-L1 of immune cells had significantly worse PFS than those with low expression of both markers. Analysis of public data (GSE17920) confirmed that high CD47 mRNA expression was associated with worse PFS (p = 0.02). Functional enrichment analyses revealed that high CD47 expression was linked to pathways involving chemokine signaling and immune cell migration, with increased infiltration of M1 macrophages, neutrophils, and eosinophils in the TME. CD47 might be involved in the disease progression and prognosis of CHL, it had a closely positive correlation with PD-L1. Targeting of CD47 and PD1/PDL1 might provide a promising strategy in CHL.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1680256"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433371","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":"CAR-Cell Therapy for Autoimmune Diseases: From the Laboratory to Clinical Practice.","authors":"Xiao-Peng Zhang, Yi-Dong Chen, Qi Yu, Fang Liu, Jia-Min Li, Shuang Li, Yi-Yu Cheng, Xiao-Yu Fu, Qian-Xi Xia, Jun-Rong Li, Xiao-Hua Hou, Liang-Ru Zhu","doi":"10.1155/jimr/6629562","DOIUrl":"10.1155/jimr/6629562","url":null,"abstract":"<p><p>Autoimmune diseases (AIDs) are characterized by a breakdown in immune tolerance, wherein the patient's immune system fails to recognize self-tissues and subsequently attacks the body's organs and tissues. Although there are many therapeutic medicines targeting the pathogenic mechanisms, there is currently a lack of curative or long-term symptom control options. Chimeric antigen receptor (CAR) cells are engineered cells that express multifunctional synthetic receptors. These CAR cells specifically target killer pathogenic immune cells and offer a novel approach to treating AIDs by modulating the immune microenvironment. Recent studies have demonstrated satisfactory outcomes with this method in managing autoimmune conditions. In our review paper, we provide a comprehensive summary of previous cases utilizing CAR cell therapy for AIDs. We hope that our review will provide clinicians with more options for the treatment of AIDs.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e6629562"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433338","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}