Journal of Immunology Research最新文献

{"title":"The Multifaceted Role of the IL-2 Cytokine Family in Melanoma: Mechanisms, Therapeutic Implications, and Immune Modulation.","authors":"Mona Daghaighei, Samaneh Dodge, Soheil Bolandi, Boutros Youssef, Niket Attarde, Moein Maddahi, Maryam Mostofi, Reza Morovatshoar, Mehrnaz Mostafavi, Dejbakht Majid, Mohammadamin Joulani, Pegah Tamimi, Malihe Sharafi, Qumars Behfar, Yasaman Ghodsi Boushehri, Alireza Azani","doi":"10.1155/jimr/8890939","DOIUrl":"10.1155/jimr/8890939","url":null,"abstract":"<p><p><b>Background and Objective:</b> Melanoma is a complex malignancy where the interplay between immune cells, cytokines, and the tumor microenvironment (TME) significantly influences disease progression and patient outcomes. This review explores the involvement of the interleukin-2 (IL-2) cytokine family in both the development and therapeutic approaches for melanoma. <b>Methods:</b> A narrative literature review was conducted, synthesizing findings from studies on immune cell behavior, cytokine functions, and their implications in melanoma and other cancers. This narrative review emphasizes the roles of immune cells and cytokines in both promoting and inhibiting tumor growth. <b>Results:</b> Neutrophils, influenced by tumor-derived cytokines, can adopt phenotypes that either inhibit or promote tumor growth. B cells in the TME often correlate with better survival, although their regulatory forms can suppress immune responses. Tissue-resident memory T cells (TRM cells) are crucial for antitumor immunity, particularly in response to immune checkpoint inhibitors (ICIs). Dendritic cells (DCs) are vital for antigen presentation, yet their function can be compromised in melanoma. Macrophages frequently support tumor growth through immunosuppressive actions. The IL-2 cytokine family, including IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21, plays diverse roles in immune regulation. These cytokines are involved in T-cell proliferation, B-cell differentiation, and modulation of other immune responses, influencing both tumor progression and the effectiveness of immunotherapies. <b>Conclusions:</b> Immune cells and cytokines are pivotal in the pathogenesis, progression, and immunotherapy of melanoma. Understanding their complex roles offers insights into potential therapeutic strategies, highlighting the importance of targeted immunotherapies in treating melanoma and possibly other cancers. Additional studies are required to clarify the precise mechanisms and interactions occurring within the TME to enhance treatment strategies.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"8890939"},"PeriodicalIF":3.5,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600693","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":"Longitudinal Analysis of Traditional Inflammatory Markers (IL-6, CRP) Juxtaposed With Heparin-Binding Protein (HBP) and Serum Amyloid A Protein Component (SAA) During Acute Infection and Convalescence From COVID-19 Infection in the Context of Initial Viral Load and Markers of Tissue Destruction.","authors":"Ahmed Sayed Ahmed, Mohamed A Mahmoud, Hossam Gad, Mohamed Antar, Abdelhamed Elgazar, Vasishta Anil, Daniel A Diedrich, Krzysztof Laudanski","doi":"10.1155/jimr/8881752","DOIUrl":"10.1155/jimr/8881752","url":null,"abstract":"<p><p><b>Purpose:</b> Characterization of immune system heterogeneity in COVID-19 patients by comparing the inflammatory markers heparin-binding protein (HBP), serum amyloid A protein (SAA), IL-6, and C-reactive protein (CRP) in relation to viral burden, immune response, and tissue damage. Also, determine if prolonged elevations in these markers are associated with long-term symptoms of COVID-19. <b>Methods:</b> This study enrolled 106 hospitalized patients with PCR-confirmed diagnoses of COVID-19. Blood samples were collected within 24 h of admission (<i>t</i> _24h), at 48 h (<i>t</i> _48h), 7 days (<i>t</i> _7d), and long-term, greater than 1 month, post discharge (<i>t</i> _LongTerm). Serum levels of HBP, SAA, IL-6, and CRP were measured using a commercial point-of-care device. Viral burden was assessed via serum viral spike S-protein serum levels and specific immunoglobulins G, M, and D against S&N proteins, and SARS-CoV-2 proteins were quantified. Tissue injury was evaluated by measuring HMGB-1 levels. Clinical data were reviewed retrospectively. Healthy individual samples served as controls. <b>Results:</b> COVID-19 patients exhibited significantly elevated serum HBP and SAA compared to healthy controls. SAA levels normalized over 1 month, whereas HBP, CRP, and IL-6 remained persistently elevated. Patients requiring intensive care unit (ICU) admission, endotracheal intubation, or extracorporeal membrane oxygen (ECMO) demonstrated higher CRP, IL-6, and HBP at initial assessment. However, after 48 h, only IL-6 was elevated in patients who subsequently expired. No significant correlations emerged between serum HBP levels and HMGB-1, viral spike protein levels, or antibodies against SARS-CoV-2 proteins. Pre-existing or acquired comorbidities did not significantly influence HBP or SAA concentrations. An analysis of biomarker profiles identified four distinct patient clusters, each characterized by unique inflammatory patterns that remained stable over time. Specifically, Cluster 1 exhibited low IL-6 with high SAA and CRP. Cluster 2 had low HBP with the highest IL-6. Cluster 3 demonstrated low SAA and CRP levels, and Cluster 4 exhibited robust inflammatory responses across all markers except IL-6. <b>Conclusions:</b> The persistence of inflammatory markers suggests ongoing inflammatory responses post-COVID-19 infection. Significant heterogeneity observed in inflammatory responses upon admission indicates multiple distinct inflammatory phenotypes, which may have implications for clinical outcomes and management strategies.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"8881752"},"PeriodicalIF":3.5,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12228567/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575537","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":"Macrophage Transcriptomic Alterations Driven by Alphavirus-Based Cancer Immunotherapy Vectors.","authors":"Ksenija Korotkaja, Darija Lapina, Zhanna Rudevica, Anna Zajakina","doi":"10.1155/jimr/6573891","DOIUrl":"10.1155/jimr/6573891","url":null,"abstract":"<p><p>Cancer cells promote the polarisation of tumour-associated macrophages (TAMs) into pro-tumorigenic M2-like phenotype, contributing to cancer progression. Reprogramming TAMs by viral immunotherapy vectors represents a promising strategy for cancer therapy. However, the factors driving macrophage reprogramming into a tumour-suppressing M1-like phenotype in response to viral vectors remain unclear. Alphaviral vectors, such as Semliki Forest virus (SFV), indirectly influence macrophages through cancer cell infection, cytokine gene delivery and tumour microenvironment (TME) modulation. This study examines macrophage transcriptomic alterations induced by SFV vectors. Murine mammary cancer cells were infected with SFV delivering tumour necrosis factor-α (TNFα) or interferon-γ (IFNγ) genes. Conditioned media from infected cells were used to treat bone marrow-derived macrophages (BMDMs) with subsequent analysis of the transcriptome. As a result, SFV-infected cancer cells significantly altered cytokine and chemokine profiles, reducing immunosuppressive factors (e.g., IL-10) and increasing inflammatory mediators (e.g., CXCL10 and CCL4). RNA sequencing revealed upregulation of genes associated with antigen presentation, interferon responses and M1 polarisation in macrophages treated with SFV/TNFα and SFV/IFNγ-conditioned media. SFV/IFNγ inhibited cancer-associated pathways (angiogenesis, glycolysis and extracellular matrix (ECM) remodelling) and enhanced cytotoxic lymphocyte (CTL) chemoattractants (CXCL9 and CXCL10). SFV/TNFα selectively upregulated <i>Mmp2</i>, <i>Mmp14</i> and <i>Ccl22</i>. All SFV vectors upregulated PD-L1 (<i>Cd274</i>) expression. The study demonstrates that alphavirus-mediated gene delivery to cancer cells can impact macrophages, inducing proinflammatory responses and reprogramming them into anti-cancer phenotype. However, combining SFV/IFNγ with immune checkpoint inhibitors could potentially improve therapeutic efficacy by mitigating virus-induced suppressive signals in the TME.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"6573891"},"PeriodicalIF":3.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12181664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475583","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 Molecular Mechanisms of Imatinib Treatment on Acute Lung Injury in Septic Mice Through Proteomic Technology.","authors":"Xiao Wang, ZhiQing Zhou, DuanYang Li, BoYang Zhang, XiaoLong Zong, Xue Liang, ZhenYu Li","doi":"10.1155/jimr/4526375","DOIUrl":"10.1155/jimr/4526375","url":null,"abstract":"<p><p><b>Background:</b> Acute lung injury (ALI) is the most common complication of sepsis. Despite considerable progress in the treatment of sepsis, the effective treatment strategies are lacking. A previous study has shown that imatinib reduces the rate of acute pulmonary damage in septic mice; however, the molecular mechanism remains unclear. Therefore, the current study aimed to investigate the potential mechanism by which imatinib alleviates ALI in septic mice. <b>Methods:</b> A septicemia model was established by intraperitoneal injection of lipopolysaccharide (LPS), followed by tail vein injection of imatinib in the treatment group. Enzyme-linked immunosorbent assay (ELISA) was used to detect inflammatory factors, and hematoxylin staining was used to detect pathological injury to the lung tissue. Tandem mass tag (TMT) quantitative labeling technology was used for proteomic sequencing analysis. The main target protein was identified through bioinformatics, and its expression was confirmed using western blotting. <b>Results:</b> We identified 128 differentially expressed proteins were associated with the protective effects of imatinib against septic lung injury. Functional enrichment analysis indicated that these proteins may be related to electron transfer, coagulation, and endothelial cell regulation in the oxidative respiratory chain. Enrichment of the nuclear factor-kappa B (NF-kB) signaling pathway, complement-coagulation cascade, and chemokine signaling pathway was also observed. Additionally, we found that the expression of CCAAT/enhancer-binding protein delta (CEBPD) and pyruvate dehydrogenase kinase 4 (PDK4) increased in the sepsis group but decreased in the imatinib group. <b>Conclusion:</b> Imatinib may reduce ALI in mice with sepsis by participating in oxidative respiratory and inflammatory responses, clotting response-related signaling pathways, and downregulating CEBPD and PDK4 expression.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"4526375"},"PeriodicalIF":3.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309995","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":"Roles of Mitochondrial Fusion and Division in Harmine Derivative H-2-168-Induced Neurotoxicity.","authors":"Yuehong Gong, Meichi Pan, Hang Ren, Dongling Peng, Meiling Zhao, Yicong Zhao, Chunlin Luo, Qin Ma, Hao Wen, Jianhua Wang","doi":"10.1155/jimr/6678026","DOIUrl":"10.1155/jimr/6678026","url":null,"abstract":"<p><p><b>Background:</b> Harmine (HM) has several pharmacological effects; however, severe neurotoxicity limits its clinical application and development. HM neurotoxicity is associated with abnormal energy metabolism. This study aimed to explore the roles and underlying mechanisms of mitochondrial fusion and division in HM derivative H-2-168-induced neurotoxicity. <b>Methods:</b> PC12 cells were treated with H-2-168, Mdivi-1 (an inhibitor of mitochondrial division), or a combination of both. Cell viability, levels of reactive oxygen species (ROS), adenosine triphosphate (ATP), lactic dehydrogenase (LDH), mitochondrial morphology, and membrane potential were measured. Immunofluorescence (IF) and western blotting were used to determine the expression of apoptosis-, mitochondrial fusion-, and division-related proteins. Additionally, PC12 cells with Drp1 knockdown or Mfn2 overexpression were generated to explore their effects. <b>Results:</b> H-2-168 alone or in combination with Mdivi-1 significantly reduced PC12 cell viability, induced apoptosis, and impaired mitochondrial function. These effects were accompanied by increased levels of ROS and LDH, reduced ATP levels, upregulation of caspase-3, cytochrome c (Cyt-c), Drp1, and Fis1, and downregulation of Mfn2 and OPA1. Additionally, Drp1 knockdown or Mfn2 overexpression further enhanced the H-2-168-induced reduction in cell viability. <b>Conclusions:</b> These data implied that H-2-168 may initiate apoptosis in PC12 cells by influencing the balance between mitochondrial fusion and division, accompanied by changes in energy metabolism, which may induce neurotoxicity.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"6678026"},"PeriodicalIF":3.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12149512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266420","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":"Monoclonal Antibodies Against Vascular Endothelial Growth Factor A (VEGF-A) Reduce Synovitis, Bone Damage, and Osteogenesis in an SKG Mouse Model of Spondyloarthritis.","authors":"Marcin Czepiel, Małgorzata Stec, Anna Gąsiorek, Anna Gałuszka, Kornelia Kłosińska, Joanna Kozieł, Jarosław Czyż, Jarosław Baran, Przemysław Błyszczuk, Maciej Siedlar, Mariusz Korkosz","doi":"10.1155/jimr/8870895","DOIUrl":"10.1155/jimr/8870895","url":null,"abstract":"<p><p>Vascular endothelial growth factor-A (VEGF-A) plays a pivotal role in inflammatory rheumatic diseases, including spondyloarthritis (SpA). Recently, we have demonstrated that the expression of VEGF-A in human classical monocytes is positively associated with the number of swollen and painful joints in SpA patients. Therefore, we tested whether the anti-VEGF-A therapy can affect the hallmarks of SpA in the SKG mouse model. When initiated at the disease onset, the administration of anti-VEGF-A monoclonal antibodies (mAbs) significantly reduced the objective symptoms of SpA in the curdlan suspension-treated mice compared to their untreated and isotypic control-treated counterparts. Micro-computed tomography (CT) imaging revealed substantial benefits of the treatment, with anti-VEGF-A mAbs-treated mice exhibiting preserved joint spaces, reduced number and depth of bone erosions, and limited new bone formation in hind paws, calcaneus, sacroiliac joints, and caudal vertebrae. These effects remained in contrast to the pronounced damage and osteogenesis in relevant skeletal regions of control animals. The histological assessment confirmed reduced synovial inflammation and bone erosions in anti-VEGF-A mAbs-treated mice, underscoring the efficacy of the treatment in mitigating SpA bone damage. Collectively, anti-VEGF-A mAbs treatment favors the maintenance of joint and spine structures, alleviates bone destruction and osteogenesis, and reduces local inflammation in the mouse SpA model. Our study pinpoints anti-VEGF-A mAb therapy as a promising avenue to understand the SpA pathogenesis and as a treatment option. It also addresses vascular and inflammatory aspects of the disease and illustrates the potential of the SKG mouse SpA model for assessing the long-term safety of anti-VEGF-A therapy before its clinical translation.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"8870895"},"PeriodicalIF":3.5,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248185","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":"Th17/Treg Cell Imbalance May Contribute to Spontaneous Preterm Labor.","authors":"Meiyi Xu, Cunling Zhang, Dan Wu, Liying Yao, Mengyuan Geng, Shanshan Li, Yuling Guo, Qiushui Wang, Zhuo Wei, Wen Li","doi":"10.1155/jimr/8405365","DOIUrl":"10.1155/jimr/8405365","url":null,"abstract":"<p><p>Spontaneous preterm labor (SPTL) is a major cause of neonatal mortality and severe complications. T cells play a crucial role in mediating inflammation and immune tolerance at the maternal-fetal interface. T helper 17 cells (Th17, pro-inflammatory) and regulatory T cells (Treg, anti-inflammatory) are two subsets of CD4⁺ T cells with opposite functions, and their balance is important for maintaining immune homeostasis. Since infection and inflammation represent prominent factors responsible for the pathogenesis of SPTL, Th17/Treg imbalance at the maternal-fetal interface may trigger proinflammatory responses, potentially leading to SPTL. In this review, evidence from both clinical cases of SPTL and animal models indicates the presence of Th17/Treg imbalance in both peripheral blood and the maternal-fetal interface. Additionally, interleukin-6 (IL-6), interleukin-1<i>β</i> (IL-1<i>β</i>), and interleukin-8 (IL-8) have been involved in the pathogenesis of inflammation-induced SPTL, suggesting that Th17/Treg imbalance may have relevance to and be involved in the pathogenic process of SPTL. Moreover, the presence of Th17/Treg imbalance in risk factors for SPTL, such as autoimmune diseases and bacterial infections, further supports this connection indirectly. Although predictive models and interventional strategies related to SPTL have been explored, there is currently insufficient evidence to establish a direct causal relationship between Th17/Treg imbalance and the onset of SPTL.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"8405365"},"PeriodicalIF":3.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12122159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182393","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":"Antiretroviral Therapy at Conception Leads to Lower Peripheral CD49a⁺ NK Cells and Higher SERPINB2.","authors":"Yanling Huo, Jinhee Kim, Deborah Kacanek, Sadia Samer, Elizabeth G Livingston, Elizabeth Stankiewicz Machado, Elena Martinelli","doi":"10.1155/jimr/4771787","DOIUrl":"10.1155/jimr/4771787","url":null,"abstract":"<p><p><b>Problem:</b> Antiretroviral therapy (ART) during pregnancy is essential to prevent vertical HIV transmission and preserve the health of the mother and child. However, ART in pregnancy has been associated with adverse birth outcomes linked to poor placental development. Immune dysregulation of placental development is an important factor in the development of preeclampsia (PE), a common hypertension disorder of pregnancy. Some studies found an association between ART use at conception or during the first trimester and PE. However, little is known regarding the impact of timing of ART initiation on the immune environment in pregnancy. <b>Methods:</b> To investigate the immune environment in pregnant persons with HIV (PPWH) on ART at conception (<i>N</i> = 40) compared to PPWH that started ART in the second trimester (<i>N</i> = 40) we analyzed specimens from the International Maternal Pediatric Adolescent AIDS Clinical Trials (IMPAACT) Perinatal Core Protocol, P1025, concluded in 2013. <b>Results:</b> No difference was found in soluble factors in circulation including PlGF and sFLt-1, associated with PE. However, upon analysis of PBMC by high dimension flow cytometry, we detected a lower frequency of circulating CD49a⁺ NK cells, associated with uterine tissue and pregnancy, in PPWH on ART at conception compared with PPWH who started ART in the second trimester. Moreover, PBMC from PPWH on ART at conception expressed higher levels of SERPINB2 in transcriptomics analyses. <b>Conclusions:</b> Our findings shed new insights into the potential impact of ART at conception and suggest the persistence of a dysregulated inflammatory environment compared to PPWH starting ART after the conclusion of placental development.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"4771787"},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174015","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 Impact of Killer Cell Immunoglobulin-Like Receptors and Human Leukocyte Antigen-E, Human Leukocyte Antigen-G Polymorphisms on Innate Immunity and COVID-19 Severity.","authors":"Cigdem Kekik, Sonay Temurhan, Yeliz Ogret, Behnoush Nasr Zanjani, Demet Kıvanc, Fatma Savran Oguz, Murat Kose, Fatma Betul Oktelik, Gunnur Deniz","doi":"10.1155/jimr/6691437","DOIUrl":"10.1155/jimr/6691437","url":null,"abstract":"<p><p><b>Background:</b> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection spans a spectrum of symptoms, ranging from mild respiratory issues to severe outcomes like pneumonia, acute respiratory distress syndrome, and fatality. Natural killer (NK) cells, governed by killer cell immunoglobulin-like receptors (KIRs), play a pivotal role in directly combating viral infections. Emerging studies indicate a decline in NK cell numbers and heightened NKG2A expression in infected individuals. <b>Objective:</b> This study focuses on genotyping human leukocyte antigen (HLA)-E, HLA-G, and KIR in SARS-CoV-2-positive individuals, comparing data between those with mild and moderate/severe symptoms. The cohort comprised 100 COVID-19-positive patients and 100 healthy volunteers, both groups subjected to DNA isolation and genotyping using sequence-based sequencing. <b>Results:</b> In 97 COVID-19-positive patients (52 mild, 24 moderate, and 21 severe) and 100 healthy volunteers, the study revealed protective associations with inhibitory alleles (KIR2DL1, KIR2DL3, KIR2DL4, KIR3DL1, KIR3DL2, and pseudo-alleles like KIR3DP1<i>⁣</i> ^<i>∗</i> 003). Conversely, predisposing factors included activator alleles (KIR2DS2, KIR3DS1) and pseudo-alleles (KIR3DP<i>⁣</i> ^<i>∗</i> 001/002). The G ^<i>∗</i> 01:04 allele and G ^<i>∗</i> 01:04-G ^<i>∗</i> 01:04 genotype emerged as protective, while the HLA-E ^<i>∗</i> 01:03-HLA-E ^<i>∗</i> 01:03 genotype may negatively impact disease prognosis. Conversely, the HLA-E ^<i>∗</i> 01:01-HLA-E ^<i>∗</i> 01:03 and HLA-E ^<i>∗</i> 01:01-HLA-E ^<i>∗</i> 01:01 genotypes may confer protection. <b>Conclusion:</b> Genetic variations in KIR, HLA-E, and HLA-G are associated with susceptibility and resistance to severe COVID-19 outcomes. This elucidates the intricate interplay of NK cells and immune-related genes, offering insights into potential therapeutic avenues and personalized approaches.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"6691437"},"PeriodicalIF":3.5,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12088842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101110","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":"RETRACTION: lncRNA PANTR1 Upregulates BCL2A1 Expression to Promote Tumorigenesis and Warburg Effect of Hepatocellular Carcinoma through Restraining miR-587.","authors":"Journal Of Immunology Research","doi":"10.1155/jimr/9874823","DOIUrl":"https://doi.org/10.1155/jimr/9874823","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2021/1736819.].</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2025 ","pages":"9874823"},"PeriodicalIF":3.5,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12066175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011036","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}