Immunologic Research最新文献

{"title":"A novel variant in the STIM1 gene leading to combined immunodeficiency and congenital myopathy.","authors":"Amirreza Taherkhani, Mahmood Gorjizad, Farzad Ahmadabadi, Mohammad Saberi, Samin Sharafian, Mehrnaz Mesdaghi, Samin Alavi, Ali Akbar Sayari, Samaneh Abdolahzadeh, Sahar Seraj, Hamidreza Hassanipour, Zahra Chavoshzadeh","doi":"10.1007/s12026-025-09642-5","DOIUrl":"https://doi.org/10.1007/s12026-025-09642-5","url":null,"abstract":"<p><p>Stromal interaction molecule 1 (STIM1) is a transmembrane protein located in the endoplasmic and sarcoplasmic reticulum, where it plays a crucial role in activating calcium release-activated calcium (CRAC) channels. It functions as a calcium (Ca²⁺) sensor within the endoplasmic reticulum (ER), triggering CRAC channel opening and allowing calcium entry-mechanisms essential for maintaining intracellular calcium homeostasis. Mutations in the STIM1 gene that impair calcium signaling can disrupt both T cell and muscle cell function, leading to combined immunodeficiency and congenital myopathy. Here, we describe a 9-year-old boy with these clinical features, who was found to carry a previously undescribed mutation in the STIM1 gene. The patient presented with recurrent pneumonia, blood-streaked diarrhea, eczema, muscle weakness, and failure to thrive. Whole exome sequencing identified a novel homozygous missense variant in STIM1 (c.584T > C | p.Leu195Pro), considered likely pathogenic. This classification was supported by high Combined Annotation Dependent Depletion (CADD) and Rare Exome Variant Ensemble Learner (REVEL) scores of 29.8 and 0.89, respectively. Homozygosity of the mutation was confirmed using PCR-Sanger sequencing. This case highlights a novel homozygous STIM1 variant in a child with combined immunodeficiency and congenital myopathy. The clinical presentation is consistent with previously reported phenotypes associated with STIM1 deficiency.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"86"},"PeriodicalIF":3.3,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"tRNA-derived fragments: biomarkers and therapeutic targets in autoimmune diseases.","authors":"Akanksha Kaimwal, Muhammed Hadish, Anil Kumar, Ajay Kumar, Anjana Munshi","doi":"10.1007/s12026-025-09639-0","DOIUrl":"https://doi.org/10.1007/s12026-025-09639-0","url":null,"abstract":"<p><p>TRNA-derived fragments (tRFs) are tiny non-coding RNAs that control gene expression and immunological responses. Initially, the tRFs were thought to be only a byproduct of Transfer RNA (tRNA) degradation. Recent studies highlighted their role in autoimmune diseases like type 1 diabetes (T1D), inflammatory bowel disease (IBD), rheumatoid arthritis (RA), sjögren's syndrome (SS) and systemic lupus erythematosus (SLE). The tRFs can influence the gene expression that are potentially involved in autoimmune diseases. The tRFs can alter immune cell function and influence the pathways that lead to autoimmune diseases. This review examines how tRFs impact immune system regulation, such as interactions with messenger RNAs (mRNA), inhibition of apoptosis, and immune cell development. Dysregulation of this leads to the progression or severity of autoimmune diseases. In addition, the potential of tRFs as biomarkers for autoimmune diseases and their targets of novel therapeutic interventions. However, this area is still in its infancy and needs more research to understand the role of a wide range of tRFs in autoimmune diseases.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"85"},"PeriodicalIF":3.3,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D deficiency and immune health in polar populations: a systematic review and hypothesis-driven narrative analysis.","authors":"Sanchit Mehta, Vansh Patel, Shrishti Agarwal, Nivedita Pant, Shikha Suman, Aibannehbok Ethan Lato Sohliya","doi":"10.1007/s12026-025-09640-7","DOIUrl":"10.1007/s12026-025-09640-7","url":null,"abstract":"<p><p>Vitamin D is essential for regulating the immune system and preventing disease, yet vitamin D deficiency is common, especially in people living in polar regions. This systematic review examines the interplay between vitamin D levels, immune function, and the unique immunological challenges faced by polar residents. Through a comprehensive review of studies, three main areas were explored: (1) the impact of vitamin D deficiency on immune responses, (2) vitamin D status in polar regions, and (3) widespread immune deficiency in polar populations. Results showed that vitamin D deficiency is associated with increased vulnerability to respiratory infections, autoimmune diseases, and inflammatory diseases, while vitamin D supplementation consistently improved immune markers and downgraded disease severity. People living in polar regions face an increased risk due to limited solar radiation, diet, and environmental stressors, which contribute to increased immunosuppression, altered cytokine profiles, and susceptibility to infections. The summary findings highlight three key factors linking vitamin D deficiency, immune deficiencies, and unique health risks in polar populations. Addressing these deficiencies may be an effective strategy to strengthen immunity and reduce disease burden in these vulnerable groups.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"84"},"PeriodicalIF":3.3,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered CD27-related T cell subsets reflect immune imbalance in systemic lupus erythematosus.","authors":"Xiaoning Chen, Bing Shen, Weijie Lin, Ziqi Xiong, Bohao Yang, Hanxi Luo, Zhiwei Zong, Jie Chen, Ayibaota Bahabayi, Chen Liu","doi":"10.1007/s12026-025-09637-2","DOIUrl":"https://doi.org/10.1007/s12026-025-09637-2","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to analyze CD27 expression in various subsets of CD4+ T cells in peripheral blood, explore the functional characteristics of the CD27+ subsets in regulatory T cells (Tregs) and CD4+ T cells, and assess their immunological alterations in newly diagnosed systemic lupus erythematosus (SLE) patients.</p><p><strong>Methods: </strong>Peripheral blood was collected from 34 newly diagnosed, untreated SLE patients and 22 healthy controls. Flow cytometry was used to analyze CD27 expression on T cell subsets, comparing the functional markers between CD27+ and CD27- subsets. CD27 expression on Tregs and total CD4+ T cells in SLE patients and healthy controls were compared. ROC curves were constructed, and areas under the curve (AUCs) was calculated to evaluate the diagnostic value of CD27-related T cell subsets for SLE.</p><p><strong>Results: </strong>The proportion of Tregs in the peripheral blood of SLE patients was increased, and CD27 expression was higher in Tregs than in CD4+ T cells in healthy individuals. CD27+ CD4+ T cells exhibited higher CD45RA and lower CD226 expression. CD27+ Tregs showed higher Helios and TIGIT expression and lower CD226 expression. CD27+ cell proportions in both CD4+ T cells and Tregs were significantly reduced in SLE patients. The AUC for CD27-related T cell subsets in diagnosing newly diagnosed SLE ranged from 0.6238 to 0.86.</p><p><strong>Conclusion: </strong>CD27⁺ CD4⁺ T cells show reduced activation features, while CD27⁺ Tregs exhibit enhanced regulatory potential. Their decreased proportions in SLE patients suggest early immune dysregulation.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"83"},"PeriodicalIF":3.3,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of nonsense variants in the ATM gene mimicking SCID phenotype: a brief report.","authors":"Sinem Firtina, Merve Saritas, Yuk Yin Ng, Serdar Nepesov, Ayca Kiykim, Selcen Bozkurt, Sevgi Bilgic-Eltan, Ozden Hatirnaz Ng, Muge Sayitoglu","doi":"10.1007/s12026-025-09638-1","DOIUrl":"https://doi.org/10.1007/s12026-025-09638-1","url":null,"abstract":"<p><p>Severe combined immunodeficiency (SCID) represents a life-threatening inborn error of immunity, necessitating rapid diagnosis and intervention to prevent fatal outcomes. While SCID is characterized by profound T-cell lymphopenia, it may overlap with other conditions like ataxia-telangiectasia (AT), which also presents with T-cell deficiencies. This study examines two cases of suspected SCID in infants, later identified as AT due to pathogenic variants in the ATM gene. Despite initial negative results from SCID-targeted gene panels, further genetic testing revealed nonsense mutations (p.Y2036X and p.E1996X) in the FAT domain of the ATM gene, confirmed by Sanger sequencing. The patients exhibited significant T-cell lymphopenia and reduced ATM protein activity, indicative of AT. These findings highlight the importance of comprehensive genetic screening beyond common SCID-associated genes, especially in patients with atypical presentations. Early and accurate diagnosis can prevent mismanagement and guide appropriate therapies, improving patient outcomes.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"82"},"PeriodicalIF":3.3,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of antipsoriatic potential of novel pemetrexed disodium-loaded transdermal patches in an imiquimod-induced mouse model.","authors":"Tejpal Yadav, Hemant Kumar Singh Yadav, Ritu Gilhotra","doi":"10.1007/s12026-025-09635-4","DOIUrl":"https://doi.org/10.1007/s12026-025-09635-4","url":null,"abstract":"<p><p>Psoriasis is a chronic autoimmune skin disorder characterized by keratinocyte hyperproliferation, inflammation, and angiogenesis, significantly impacting patients' quality of life. Current therapeutic strategies, including topical corticosteroids, phototherapy, and systemic biologics, often present limitations such as adverse effects, high costs, and inadequate skin penetration. Transdermal drug delivery offers a promising alternative by enhancing localized drug bioavailability and minimizing systemic side effects. In this study, we investigated the antipsoriatic potential of pemetrexed disodium, a multitargeted antifolate agent, formulated as a transdermal patch in an imiquimod-induced psoriasis mouse model. The patches were prepared using a solvent evaporation technique and optimized for controlled drug release. Mice treated with pemetrexed-loaded transdermal patches exhibited significant dose-dependent reductions in psoriasis severity, as evidenced by improvements in Psoriasis Area and Severity Index (PASI) scores, histopathological analysis, and suppression of inflammatory cytokines (TNF-α, IL-6) assessed via qRT-PCR and ELISA. The highest concentration (0.16 mg/cm²) demonstrated the most pronounced therapeutic effects, comparable to the standard ketoconazole treatment. These findings highlight the potential of pemetrexed disodium-loaded transdermal patches as an innovative, targeted therapy for psoriasis, warranting further clinical investigations.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"81"},"PeriodicalIF":3.3,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chrysin-loaded poly (lactic-co-glycolic acid) nanoparticles alleviate sepsis-induced splenic injury by regulating myeloid-derived suppressor cells.","authors":"Islam Ahmed Abdelmawgood, Abeer Mahmoud Badr, Asmaa Elsayed Abdelkader, Noha A Mahana, Ayman Saber Mohamed, Hadeer Hesham Abdelfattah","doi":"10.1007/s12026-025-09634-5","DOIUrl":"https://doi.org/10.1007/s12026-025-09634-5","url":null,"abstract":"<p><p>Sepsis is a serious condition resulting from a dysregulated immune-mediated response to an infection. Myeloid-derived suppressor cells (MDSCs) aggregate and serve a protective function in the pathophysiology of lipopolysaccharide (LPS) shock. However, the regulation of MDSCs by chrysin-loaded poly (lactic-co-glycolic acid) (PLGA) nanoparticles (CHR-NP) remains unexplored. CHR-NP was synthesized and characterized by Fourier transform infrared (FTIR) spectroscopy, transmission electron microscopy (TEM), zeta potential, and dynamic light scattering (DLS). Before being given an intraperitoneal injection of 10 mg/kg of LPS, C57BL/6 mice were given CHR (50 mg/kg), PLGA (50 mg/kg), CHR-NP (50 mg/kg), and dexamethasone (Dexa) (5 mg/kg) by oral administration for 6 days. CHR-NP effectively mitigated LPS-induced splenic injury by diminishing inflammation and oxidative stress. The CHR-NP treatment lowered the amount of malondialdehyde (MDA) and raised the levels of antioxidants like glutathione (GSH), catalase (CAT), and glutathione peroxidase (GPx). Besides that, it stopped the production of cytokines that cause inflammation (tumor necrosis factor (TNF)-α, IL-1β, interferon (IFN)-γ, and IL-12) and increased the production of cytokines that stop inflammation (IL-10 and IL-4). This study demonstrates that CHR-NPs confer significant protective effects against LPS-induced sepsis by modulating immune responses, reducing oxidative stress, and alleviating splenic injury. The ability of CHR-NP to enhance antioxidant defenses, suppress pro-inflammatory cytokines, and promote anti-inflammatory mediators highlights its potential as a novel therapeutic approach for regulating MDSCs and mitigating sepsis-related immunopathology.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"80"},"PeriodicalIF":3.3,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of anti-neutrophil extracellular traps (NET) antibodies according to systemic lupus erythematosus clinical phenotypes.","authors":"Daniel Alberto Carrillo-Vázquez, Jennifer Tiaré Balderas-Miranda, Rosa Icela Arvizu Rivera, Alfredo Pérez-Fragoso, Beatriz Alcalá-Carmona, Miroslava Nuñez-Aguirre, Ana Sofía Vargas-Castro, Abdiel Absalón-Aguilar, Jaquelin Lira-Luna, Nancy R Mejía-Domínguez, Guillermo Juárez-Vega, Karina Santana-de Anda, Jiram Torres-Ruiz, Diana Gómez-Martín","doi":"10.1007/s12026-025-09636-3","DOIUrl":"https://doi.org/10.1007/s12026-025-09636-3","url":null,"abstract":"<p><p>Anti-neutrophil extracellular traps (NETs) antibodies have been observed in patients with lupus nephritis and may contribute to the pathogenic role of NETs in patients with systemic lupus erythematosus (SLE). However, the prevalence of anti-NETs antibodies and their relationship with clinical features of patients with SLE have not been thoroughly studied, which is the aim of this study. Eighty-seven patients who fulfilled the 2019 EULAR/ACR Classification criteria for SLE were included. Plasmatic neutrophil elastase-DNA complexes as NETs remnants and the IgG anti-NETs antibodies were quantified by ELISA in the same sample. Thirty-one (35.6%) patients had positive anti-NETs antibodies. Patients with anti-NETs antibodies were younger at the time of recruitment (28.7 years (23.8-33.2) vs. 35.58 (27.88-45.77), p = 0.003) and had more prominent serological disease activity, with a higher prevalence of positive anti-double stranded (ds)-DNA antibodies (29 (93.5%) vs. 41 (73.2%), p = 0.022), higher titers (148.2 mg/dL vs. 35.6 mg/dL, p = 0.015), and lower levels of C3 and C4 (58 (37-85.5) vs. 77 (54-127), p = 0.017) and C4 (8 (8-12.5) vs. 20 (9-27), p < 0.001). From all clinical manifestations present at the time of recruitment, serositis showed a trend towards anti-NETs positivity (p 0.06). The global SLEDAI-2 K score was higher in the patient's IgG anti-NETs antibodies positive (13 (6.5-18) vs. 6 (4-15), p = 0.042). Anti-NETs antibodies were positively correlated with the systemic lupus erythematosus disease activity index (SLEDAI-2 K) score as well as with the titers of anti-dsDNA antibodies. IgG anti-NET antibodies were found in one-third of SLE patients. This is the first description of the association between IgG anti-NET and clinical features of SLE. Their characterization might allow us to address their role as potential novel biomarkers.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"79"},"PeriodicalIF":3.3,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MOSPD2 regulates the activation state of αLβ2 integrin to control monocyte migration: applicability for treatment of chronic inflammatory diseases.","authors":"Yaniv Salem, Niva Yacov, Pinhas Kafri, Oshrat Propheta-Meiran, Arnon Karni, Nitsan Maharshak, Victoria Furer, Ori Elkayam, Itzhak Mendel","doi":"10.1007/s12026-025-09633-6","DOIUrl":"https://doi.org/10.1007/s12026-025-09633-6","url":null,"abstract":"<p><p>Monocytes are innate immune cells that drive the chronicity of various inflammatory diseases. Monocyte migration to inflamed tissues involves multiple steps of interaction with the vascular endothelium and the extracellular matrix (ECM), a process mediated through conformational transitions in cell surface integrins. We previously described motile sperm domain-containing protein 2 (MOSPD2) as a surface protein expressed on myeloid cells that is essential for the migration of monocytes and a key regulator of inflammation. Investigating MOSPD2's mechanism of action, we assessed whether it plays a role in regulating integrin activation and monocyte adhesion. Data show that silencing of MOSPD2 expression in the THP-1 monocytic cell line significantly increased cell adhesion to various ECM molecules. Employing IW-601, a humanized anti-human MOSDP2 monoclonal antibody, on primary human monocytes increased adhesion to ECM molecules as well as to adhesion molecules. At the molecular level, silencing of MOSPD2 or blocking MOSPD2 using IW-601 led to a transition in integrin αLβ2 (CD11a/CD18, LFA-1) conformation into an active high-affinity binding form and to the induction of adhesion-associated signaling pathways. Co-immunoprecipitation experiments showed that MOSPD2 binds integrin-β2 (CD18), but not integrin-β1 (CD29). Our results reveal a novel mechanism controlling monocyte migration, in which MOSPD2 acts as an adhesion checkpoint that governs the balance between monocyte adhesion and release. By demonstrating the inhibitory effect of IW-601 on the migration of primary monocytes isolated from patients with chronic inflammatory diseases, we provide proof of concept for translating MOSPD2's mechanism into a potential treatment for inflammatory diseases, further supported by in vivo data in models of RA and IBD.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"78"},"PeriodicalIF":3.3,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study of immunological and inflammatory gene response in Indian cohort of COVID- 19 patients by NanoString technology.","authors":"Sudarson Sundarrajan, K N Sridhar, Manju Moorthy, Gopalakrishna Ramaswamy","doi":"10.1007/s12026-025-09626-5","DOIUrl":"https://doi.org/10.1007/s12026-025-09626-5","url":null,"abstract":"<p><p>COVID- 19, which has affected millions of people across the globe as a pandemic, is caused by the SARS-Cov- 2 virus which has a case fatality rate of 2.3%. The clinical outcome of those who had mild and severe infection exhibited different responses for the treatment due to differences in the host immune system. Predicting immune response with reliable biomarkers to monitor the severity and also identifying potential biomarkers that could help the clinician in decision-making would be important and also beneficial for the management of COVID- 19 in the hospital setup. In our study, we have used the NanoString nCounter gene expression assay to investigate the molecular signalling of host to COVID- 19 infection. The nCounter gene expression assay identified 29 genes that were differentially regulated and specific to COVID- 19 infection; out of which, 9 genes (ICAM3, PTAFR, CEACAM6, GBP1, C7, STAT1, CEACAM8, IL16, HLA-DPB1) exhibited strong predictive performance to differentiate COVID- 19 infection from healthy controls (AUC ≥ 0.9). We also observed that three genes (MAP4 K1, CTLA4, and HLA-DQB1) were able to differentiate COVID- 19 from patients with flu-like symptoms. A group of 11 genes (C2, CD14, CDKN1 A, CMKLR1, CYBB, HLA-A, IFNA2, LAG3, MARCO, TLR7, and IL15) showed a dysregulation trend with onset of COVID- 19 infection and settled to normal levels by day 14 as patient recovered. The outcome of our study may help in understanding the host immune response towards COVID- 19 infection.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"77"},"PeriodicalIF":3.3,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}