ImmunoHorizons最新文献

{"title":"Weakened macrophage antibacterial capacity in myelodysplastic syndrome.","authors":"Johnathon B Schafer, Kenneth C Malcolm, Jessica Dell-Martin, Maria L Amaya, Daniel A Pollyea, Scott Alper","doi":"10.1093/immhor/vlag037","DOIUrl":"10.1093/immhor/vlag037","url":null,"abstract":"<p><p>Patients with myelodysplastic syndrome (MDS) are immunocompromised and are therefore susceptible to fatal infection. While neutropenia and neutrophil dysfunction account for much of this immunodeficiency, other immune cells likely also contribute. In contrast to the extensive study of neutrophils in MDS, there has been very little investigation of macrophage host defense function in MDS. In the current study, we find that macrophage differentiation and macrophage phagocytosis of bacteria are greatly weakened in patients with MDS, regardless of patient genotype. Moreover, we find that killing of those bacteria that are ingested is diminished in MDS patients with high-risk disease. Using a mouse model that expresses the MDS-associated U2AF1-S34F mutation, we find that this mutation is sufficient to induce macrophage functional defects. We conclude that macrophage host defense defects likely contribute to the immunodeficiency present in MDS.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13378455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148474859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of genetic variants in B cell expressed genes associated with systemic lupus erythematosus in African American females.","authors":"Rachel Kidwell, Mansi Gupta, Jake Fontaine, Ignacio Sanz, Christopher D Scharer","doi":"10.1093/immhor/vlag029","DOIUrl":"10.1093/immhor/vlag029","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by dysregulated B cell responses and pathogenic autoantibody production. Given the central role that B cells play in SLE pathogenesis, we aimed to characterize genetic variation within the B cell compartment of African ancestry (AFR) women with SLE who are disproportionately and more severely affected by SLE. Here, we analyzed RNA-seq data from a previously published study of high disease activity AFR SLE individuals and healthy controls (HC) to identify coding variants in B cells with potential functional consequence that may underpin disease. In this cohort, we identified 575 missense variants associated with 158 unique genes. While many variant-containing genes did not exhibit large transcriptional changes between cohorts, a subset occurred within genes involved in B cell signaling, activation, and differentiation. However, genes enriched in AFR SLE were consistently upregulated across multiple B cell subtypes, suggesting that variant-associated transcriptional changes occur broadly across the B cell compartment and not within a single subset. Among these, the TNFAIP3 variant rs2230926 was enriched in AFR SLE individuals and occurs at a substantially higher allele frequency in AFR populations. This study provides insights into genetic variation found within the B cell compartment that may contribute to immune dysregulation and disease pathogenesis in SLE in AFR populations.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13387164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148551720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined transcriptomic and lipidomic analysis reveals enhanced lipogenesis in memory Tregs upon TCR activation.","authors":"Yohei Sato","doi":"10.1093/immhor/vlag035","DOIUrl":"10.1093/immhor/vlag035","url":null,"abstract":"<p><p>Regulatory T cells (Tregs) maintain immune homeostasis in vivo. Similar to conventional T cells (Tconvs), Tregs are divided into naïve and memory cells. Tregs have unique metabolic properties, including enhanced oxidative phosphorylation. The lipidomic profiles of human Tregs have been studied previously; however, those of naïve and memory Tregs have not yet been consistently compared. Thus, in the present study, we used a combined transcriptomic and lipidomic analysis to assess the metabolic features of human naïve and memory Tregs upon activation. Using transcriptomic analysis, we identified distinct gene expression profiles in naïve and memory Tregs compared with those in Tconvs. Upon TCR stimulation, memory Tregs showed a lipidomic profile distinct from that of memory Tconvs, whereas the lipidomic profiles of naïve Tregs were similar to those of naïve Tconvs. Furthermore, upon TCR stimulation, memory Tregs expressed triglycerides (TGs) that were more enriched in monounsaturated fatty acids and polyunsaturated fatty acids (PUFAs) than those of memory Tconvs. However, memory Tconvs also had higher PUFA-TG levels than naïve Tconvs and Tregs after TCR stimulation, although their levels remained lower than those in memory Tregs. These findings suggest PUFA-TGs could be a marker of memory Tregs. In turn, higher frequency of memory cells within the Treg population may also contribute to the observed enrichment of PUFA-TGs in Tregs upon TCR activation. Our study demonstrated unique transcriptomic and lipidomic profiles and enhanced lipogenesis in memory Tregs upon TCR stimulation.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148427351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CFTR modulators exert subset-specific phenotype remodeling on circulating neutrophils in cystic fibrosis.","authors":"François Chable de la Héronnière, Théo Dhôte, Rodrigo de Oliveira Formiga, Lucile Regard, Giovanni Saraceni-Tasso, Muriel Andrieu, Souganya Many, Jennifer Da Silva, Frédéric Pène, Clémence Martin, Maha Zohra Ladjemi, Pierre-Régis Burgel, Véronique Witko-Sarsat","doi":"10.1093/immhor/vlag030","DOIUrl":"10.1093/immhor/vlag030","url":null,"abstract":"<p><p>A key aspect of cystic fibrosis pathophysiology is the significant role played by neutrophils, central to the inflammatory response in cystic fibrosis airways. Neutrophil-dominated inflammation greatly influences clinical outcomes, including airway damage and lung function decline. People with cystic fibrosis have an increase in circulating neutrophils that exhibit numerous functional and phenotypic abnormalities. We used spectral flow cytometry to delineate the expression of 24 cell surface markers on neutrophils from 24 healthy donors and 45 adults with cystic fibrosis, before and after elexacaftor-tezacaftor-ivacaftor treatment. This comprehensive analysis examined phenotypic markers associated with fundamental neutrophil functions, including differentiation, maturity, activation, antimicrobial activities (degranulation, pathogen sensing and chemotaxis), metabolism, and immunomodulation. Prior to treatment, neutrophils from adults with cystic fibrosis displayed a phenotype suggestive of immune activation and metabolic aberration. Treatment with elexacaftor-tezacaftor-ivacaftor normalized a FPR1high/CXCR2high subset, an observation consistent with enhanced pathogen-sensing capacity. The treatment, however, failed to restore fully normal phenotypes in cystic fibrosis neutrophils but rather induced the modulation of a PD-L1high/CD114high/GLUT-1high subset of mature neutrophils with an increased expression of PD-L1 and adhesion molecules such as CD11c and CD11b. Taken together, our data reveal a specific immunophenotypic signature of neutrophils in cystic fibrosis that is further modified by treatment with elexacaftor-tezacaftor-ivacaftor, suggesting the opportunity for developing adjunctive therapies to enhance beneficial antimicrobial subsets while simultaneously mitigating immunosuppressive phenotypes, thereby opening new perspectives for immune modulation in cystic fibrosis treatment.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13426474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148649946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semaphorin 3E regulates the response of regulatory T cells to lipopolysaccharide-induced systemic inflammation.","authors":"Sina Taefehshokr, Ifeoma Okwor, Lianyu Shan, Abdelilah S Gounni","doi":"10.1093/immhor/vlag031","DOIUrl":"10.1093/immhor/vlag031","url":null,"abstract":"<p><p>Sepsis is a life-threatening systemic inflammation marked by an initial hyperinflammatory phase. Tregs are pivotal in tempering this early immune response. Semaphorins, originally neuronal guidance cues, have emerged as immune modulators. Notably, Sema3E influences dendritic cell and T cell responses, but its role in Treg-mediated regulation during endotoxemia is unclear. WT and Sema3e-/- mice were subjected to LPS-induced endotoxemia. Treg frequencies, proliferation and migration were assessed by flow cytometry and Transwell assays, respectively. Serum cytokines (eg IL-10) were quantified using ELISA. A TNFRSF25 agonist was administered to expand Tregs in vivo, and adoptive transfers of WT or Sema3e-/- Tregs were performed. Clinical scores and survival were recorded. Sema3e-/- mice exhibited significantly impaired Treg expansion and proliferation, altered migratory patterns with reduced Treg accumulation in spleen and lymph nodes, and consequently lower serum cytokine levels (eg IFN-γ) compared to WT, correlating with exacerbated disease severity. DR3-mediated Treg expansion in Sema3e-/- mice did not improve their clinical outcomes. Furthermore, adoptively transferred Sema3e-/- Tregs failed to confer protection in endotoxemic recipients, unlike WT Tregs. Sema3E is essential for optimal Treg responses and immune regulation during severe LPS-induced inflammation. Its absence compromises Treg expansion, localization, and function, worsening sepsis outcomes. These findings highlight Sema3E as a critical component of Treg-mediated immunosuppression and a potential therapeutic target for improving immune homeostasis in sepsis.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13401822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148595274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Medium chain fatty acid sensing receptor GPR84 limits antitumor immunity mediated by CD4 T cells in mice.","authors":"Anamaria Morales-Alvarez, Timothy A Gilbertson, Hung Nguyen","doi":"10.1093/immhor/vlag039","DOIUrl":"10.1093/immhor/vlag039","url":null,"abstract":"<p><p>CD4+ T cells play an important role in antitumor immunity due to their capacity to acquire highly functional effector states and cytotoxic-like programs in the tumor microenvironment. However, the mechanisms underlining this process remain largely undefined. Herein, we identify the medium chain fatty acid-sensing receptor GPR84 as a metabolic checkpoint that restricts the antitumor immunity mediated by CD4+ T cells. GPR84 upregulation was detected in tumor-infiltrating CD4+ T cells, and in the absence of GPR84, CD4+ T cells exhibited enhanced tumor control, associated with increase in their proliferation and survival, and with a reprogramming toward a more functionally competent state characterized by increased polyfunctional cytokine production and reduced expression of inhibitory receptors, without accumulation of regulatory T cells. In the tumor antigen-specific mouse model, GPR84 deficiency drastically improved the therapeutic efficacy of adoptively transferred CD4+ T cells. Mechanistically, without GPR84, CD4+ T cells, by upregulating mTORC1 signaling activity, metabolically enhance both glycolysis and mitochondrial activities, thereby gearing toward tumor-killing cytotoxic phenotypes. Importantly, pharmacologic inhibition of GPR84 drastically improves the effectiveness of both PD-1 blockade therapy and adoptive cell transfer. Together, these findings validate GPR84 as a key regulator of CD4+ T-cell metabolic fitness and establish the extracellular lipid sensing pathway as a targetable axis for improving the efficacy and responsiveness of cancer immunotherapies.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13355590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148427331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intermittent fasting alters the antigen-specific CD5+ B-1 cell natural antibody repertoire in male and female mice.","authors":"Sarah E Webster, Jordan Terry, Naomi L Tsuji, Daken Heck, Nichol E Holodick","doi":"10.1093/immhor/vlag038","DOIUrl":"10.1093/immhor/vlag038","url":null,"abstract":"<p><p>Natural antibodies (NAbs), primarily produced by CD5+ B-1 cells, provide critical early protection against infections such as Streptococcus pneumoniae. The structure of these natural antibodies, germline-like with minimal N-additions, is essential for their protective capacity. The protective capacity and germline status of NAbs are compromised in aged male mice but maintained in aged female mice. CD5+ B-1 cells are maintained through self-renewal, necessary for maintaining germline-like natural antibodies, and this process depends on autophagy. Intermittent fasting enhances autophagy and stem cell self-renewal, suggesting that it may influence B-1 cell persistence and natural antibody structure. Young (4-wk-old) male and female mice were placed on a fasting regimen (24-h fast weekly) or fed ad libitum for 12 wk. Here, we show that intermittent fasting modulates the antigen-specific natural IgM repertoire of young male and female mice, altering both peritoneal and splenic phosphatidylcholine-specific CD5+ B-1 cell repertoires, with the most pronounced effects in the spleen. Intermittent fasting increased the prevalence of germline-like (few N-additions) antibodies and led to an increase in VH11 usage, a variable gene mainly utilized during fetal development. Fasting also affected components of the serum repertoire; however, these effects differed between male and female mice. Female mice showed a significant decrease in phosphorylcholine- and pneumococcal polysaccharide serotype 3-specific IgM levels, whereas male mice showed a significant increase in phosphatidylcholine-specific IgM levels. We also observed a significant decrease in splenic CD5+ B-1 cells and serum interleukin-5 levels after fasting. These results suggest that intermittent fasting may help preserve or restore protective NAbs.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13378454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148474871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pglyrp1-Cre marks distinct epithelial and immune lineages across mucosal sites.","authors":"Samuel Alvarez-Arguedas, Michael U Shiloh","doi":"10.1093/immhor/vlag033","DOIUrl":"10.1093/immhor/vlag033","url":null,"abstract":"<p><p>Mucosa-associated lymphoid tissue (MALT) initiates immune responses at mucosal entry sites. Within MALT, microfold (M) cells sample luminal Ags and deliver them to underlying immune cells. Despite their functional importance, few tools enable selective manipulation of M cells in vivo. Here we report the generation and characterization of a peptidoglycan recognition protein 1 (Pglyrp1)-Cre knock-in mouse designed to provide conditional genetic access to M cells. Using Rosa26-tdTomato reporter mice, we found strong Pglyrp1 promoter activity in gut epithelial cells, including goblet and M cells, whereas activity in nasal-associated lymphoid tissue (NALT) was more heterogeneous and skewed toward immune cells, particularly neutrophils. To functionally interrogate Pglyrp1-expressing cells, we performed Cre-mediated ablation using 3 DTA-based models. The Rosa26GFP-DTA line caused marked perinatal lethality in double-positive pups, suggesting essential roles for Pglyrp1-positive cells early in life. In contrast, Rosa26DTA and Rosa26iDTR crosses produced minimal depletion of mucosal populations, including M cells, even at the highest nonlethal diphtheria toxin dose. These findings demonstrate differential Pglyrp1 promoter activity across mucosal tissues and highlight challenges in achieving M cell-specific targeting. Although not M cell-restricted, the Pglyrp1-Cre mouse provides a useful tool for manipulating Pglyrp1-expressing lineages and probing their roles in mucosal homeostasis and immunity.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13312118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148347886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An early protective effect of IL-9 in murine systemic lupus erythematosus.","authors":"Maya S Krishnan, Baohua Zhou, Dongming Yang, Joao I Goncalves, Kaitlyn G Jackson, Gloria R Xue, Matthew J Turner, Mark H Kaplan","doi":"10.1093/immhor/vlag024","DOIUrl":"10.1093/immhor/vlag024","url":null,"abstract":"<p><p>Systemic lupus erythematosus (SLE) is a progressive antibody-mediated autoimmune disease characterized by systemic immune complex deposition. A subset of SLE patients has elevated CD4+IL-9+ T cells as well as increased levels of secreted interleukin (IL)-9 and IL9 messenger RNA compared with healthy control subjects. However, because IL-9 can have both pro- and anti-inflammatory effects in autoimmune disease, its function in SLE is unclear. We use the MRL/lpr murine model of SLE to demonstrate that IL-9 exhibits protective activity in the early stages of disease. Treatment of these mice with an IL-9 neutralizing antibody from 6 to 12 wk of age results in an expansion of immune cells, leading to exacerbation of disease. In contrast, treatment with anti-IL-9 from 6 to 18 wk of age does not significantly alter disease course compared with isotype control. Anti-IL-9 antibody treatment of these mice results in reduced systemic IL-2 levels, IL-9+ type 2 innate lymphoid cells, and regulatory T cells in the kidney, suggesting an IL-9-dependent suppressive cellular circuit similar to that observed in rheumatoid arthritis. Importantly, supplementation of IL-2 during IL-9 blockade recovers regulatory T cell numbers and limits disease. Together, these data demonstrate an IL-9-dependent suppressive circuit that is evident early in the development of SLE which may be amenable to manipulation to achieve a therapeutic benefit.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13274542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148274441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRPγ limits effector differentiation of human CD8 T cells in response to subthreshold TCR-signaling.","authors":"Megan Morse, Xanthie Rodriguez, Erika Delarosa, Sierra Rodriguez, Juma Shanil, Sushmita Sinha","doi":"10.1093/immhor/vlag027","DOIUrl":"10.1093/immhor/vlag027","url":null,"abstract":"<p><p>Signal regulatory protein gamma (SIRPγ) is a T cell-specific surface receptor in the human immune system with previously undefined function in human CD8 T cell differentiation. We report that SIRPγ expression varies substantially across individuals and stratifies CD8 T cell differentiation states. Individuals with low SIRPγ expression exhibit an increased frequency of CD27-CD45RO+ effector-like and CD27-CD45RO- terminally differentiated CD8 T cells, while high expressors retain a predominance of naïve and central memory cells. To investigate the functional role of SIRPγ, we performed small interfering RNA-mediated knockdown in naïve human CD8 T cells. Under suboptimal TCR stimulation, SIRPG knockdown drove robust effector-like differentiation marked by increased CD45RO expression, T-bet upregulation, and enhanced production of TNF-α, IFN-γ, and granzyme B. This phenotype was not recapitulated by CD47 blockade, indicating that SIRPγ modulates differentiation through a CD47-independent mechanism. These findings identify SIRPγ as a negative regulator of CD8 T cell effector programming under limiting stimulatory conditions. Interindividual variability in SIRPγ expression may influence immune homeostasis and susceptibility to immunopathology, highlighting SIRPγ as a potential therapeutic target in settings of dysregulated T cell responses.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13283423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148298148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}