Immunopharmacology and Immunotoxicology最新文献

{"title":"Immunomodulatory activity of phenylephrine on LPS stimulated macrophages.","authors":"Esra Aydemir, Sude Yasemin Uran, Nur Ekimci Gürcan, Ayse Zehra Aroğuz, Furkan Ayaz","doi":"10.1080/08923973.2026.2702339","DOIUrl":"10.1080/08923973.2026.2702339","url":null,"abstract":"<p><strong>Background: </strong>Phenylephrine (PE) acts as a sympathomimetic vasoconstrictor frequently utilized to alleviate nasal blockage <i>via</i> the activation of α-1-adrenergic receptors. This study primarily sought to investigate the drug's potential to influence immune system responses.</p><p><strong>Methods: </strong>The effect of phenylephrine was analyzed by comparing cytokine production levels in LPS-stimulated and unstimulated J774.1 macrophages. The changes in concentrations of IL-6, TNF-α, IL-12p40, and GM-CSF induced by phenylephrine were measured by ELISA.</p><p><strong>Results: </strong>PE exhibited no intrinsic pro-inflammatory activity, as basal levels of TNF-α, IL-12p40, IL-6, and GM-CSF remained at or near detection limits in PE-only groups. In LPS-stimulated cultures, PE significantly attenuated the inflammatory response across multiple pathways, though the inhibitory patterns varied by cytokine. PE induced a robust, non-dose-dependent inhibition, reducing levels by 40-45% across all concentrations (<i>P</i> < 0.05). A significant dose-dependent suppression was observed, with the maximal dose (10 µg/mL) reducing levels from 9,258 pg/mL to 5,802 pg/mL (<i>P</i> < 0.05). Inhibition followed a non-monotonic trend; concentrations of 1 and 10 µg/mL significantly lowered IL-6 (<i>P</i> < 0.05), while the intermediate 5 µg/mL dose yielded no significant effect. PE mediated modulation was restricted, with significant inhibition occurring only at the highest concentration (10 µg/mL; <i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>The results indicate that phenylephrine influences inflammatory cytokine production and may have potential clinical relevance regarding immune responses and inflammatory diseases.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"760-766"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148430208","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":"A closer insight into the molecular effect of canagliflozin on gentamicin-induced nephrotoxicity in rats: attention to SIRT1/Nrf2/HO-1, p38 MAPK/NF-κB signaling pathways, and expression of miR-21 and miR-155.","authors":"Manar A Gamaan, Heba S Zaky, Hebatalla I Ahmed","doi":"10.1080/08923973.2026.2713468","DOIUrl":"10.1080/08923973.2026.2713468","url":null,"abstract":"<p><p><b>Objective:</b> Nephrotoxicity is considered the most detrimental effect of gentamicin (GM). In this study, we investigated the potential effects for canagliflozin (CANA) to protect against GM-induced nephrotoxicity, besides the multiple molecular pathways underlying these effects.<b>Methods:</b> Four groups with six rats in each were used: control; GM (100 mg/kg, intraperitoneal injection) for 7 days; CANA + GM group: Rats were given CANA (10 mg/kg, by oral gavage) for 14 days, and GM (100 mg/kg, by IP) was co-administered with CANA in the last 7 days; and CANA group: Rats were given CANA (10 mg/Kg, by oral gavage) for 14 days.<b>Results</b>: Relative to GM-challenged rats, CANA ameliorated GM-induced changes in the state of oxidative stress. Also, CANA alleviated the GM-evoked reduction in the renal expression of SIRT1 and Nrf2. Furthermore, CANA decreased the renal expression of NF-ҡB and reduced p38-MAPK levels in kidneys of GM-treated animals. Simultaneously, GM-induced changes in the renal expression of miR-21 and miR-155 have been successfully amended by CANA.<b>Conclusion:</b> Altogether, current outcomes imply that modification of the SIRT1/Nrf2/HO-1, the p38-MAPK/NF-ҡB pathways, and microRNAs (miRNAs) play an important role adressing CANA's 'protective properties against GM nephrotoxicity.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"870-881"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663762","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":"Toxic effects and mechanisms of methyl 4-hydroxybenzoate in allergic rhinitis: a multi-omics and toxicology study.","authors":"Tiantian Wang, Wenqiang Xu, Hui Wang","doi":"10.1080/08923973.2026.2705917","DOIUrl":"10.1080/08923973.2026.2705917","url":null,"abstract":"<p><strong>Purpose: </strong>Exogenous chemical exposure is closely associated with allergic rhinitis (AR). Methyl 4-hydroxybenzoate (MeP), a widely used preservative, poses risks of long-term human exposure. This study aimed to explore the potential association between MeP and AR as well as its underlying molecular characteristics.</p><p><strong>Methods: </strong>Integrating toxicological assessment, bioinformatics analysis, and machine learning approaches, this study identified overlapping targets between MeP and AR using transcriptomic data from AR patients (GSE118243, GSE43523) in the GEO database through multi-platform prediction. Subsequently, key targets were identified through differential expression analysis, functional enrichment, PPI network construction, and three machine learning approaches (Boruta, SVM, and Lasso). Further validation was performed using immune infiltration analysis, GSEA, molecular docking, and qRT-PCR experiments.</p><p><strong>Results: </strong>MeP exhibits moderate lipophilicity, low bioaccumulation potential, and toxic effects on specific organisms. Identify ESR2, IL2, and SLC3A2 as key targets, with significant expression differences (<i>p</i> < 0.05) validated in independent datasets and clinical samples. Immune infiltration analysis suggests MeP may contribute to AR progression by modulating the proportions of B cells, M2 macrophages, neutrophils, and other immune cells. GSEA reveals that key targets are enriched in pathways related to metabolism, inflammation, and autophagy.</p><p><strong>Conclusion: </strong>Bioinformatics analyses suggest that MeP is correlated with AR development, and this correlation may involve the modulation of ESR2, IL2, and SLC3A2, as well as influences on immune cell infiltration and related signaling pathways.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"844-856"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630362","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":"Repurposing the third-generation EGFR inhibitor osimertinib to synergize with paclitaxel and extend survival in anaplastic thyroid cancer.","authors":"Ran Jie, Xiawei Shen","doi":"10.1080/08923973.2026.2735423","DOIUrl":"https://doi.org/10.1080/08923973.2026.2735423","url":null,"abstract":"<p><strong>Background: </strong>Anaplastic thyroid cancer (ATC) is a highly aggressive malignancy with limited therapeutic options and poor prognosis. This study aimed to identify effective targeted agents and evaluate their therapeutic potential in combination with paclitaxel.</p><p><strong>Methods: </strong>High-throughput drug sensitivity and resistance screening was performed using a comprehensive library of targeted agents in ATC cells. The antitumor efficacy of selected agents was evaluated through <i>in vitro</i> combination studies and <i>in vivo</i> tumor models. Molecular mechanisms were investigated by assessing EGFR/ERK and eIF4E signaling. EGFR and eIF4E expression was quantified by ELISA in 24 pairs of matched ATC and adjacent non-tumor tissues.</p><p><strong>Results: </strong>Osimertinib emerged as the most potent agent in the screening and exhibited synergistic activity with paclitaxel <i>in vitro</i>, with combination index values below 1.0. <i>In vivo</i>, osimertinib significantly inhibited tumor growth and suppressed EGFR/ERK signaling and the eIF4E-mediated translational pathway. Combination treatment markedly prolonged survival, with the last observed death occurring on Day 65, compared with 100% mortality by Day 23 in vehicle-treated controls, without observed systemic toxicity. Analysis of patient tissues revealed increased EGFR and eIF4E expression in 83% and 71% of ATC cases, respectively, with co-overexpression in 58%.</p><p><strong>Conclusions: </strong>Osimertinib demonstrates potent antitumor activity in ATC, with enhanced efficacy when combined with paclitaxel. Concurrent suppression of EGFR/ERK and eIF4E-associated signaling provides a mechanistic rationale for this combination, supporting further investigation of its therapeutic potential in ATC.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-8"},"PeriodicalIF":3.1,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024579","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":"Oral tolerance induced by ovalbumin modulates the cytokine profile and increases the frequency of CD4⁺FoxP3⁺Helios⁺ Tregs expressing the GARP/LAP late-stage activation markers in antigen-stimulated cells of <i>P.paulista</i> wasp venom-sensitized mice.","authors":"Luís Gustavo Romani Fernandes, Júlia Martins Lother, Ricardo de Lima Zollner","doi":"10.1080/08923973.2026.2716674","DOIUrl":"https://doi.org/10.1080/08923973.2026.2716674","url":null,"abstract":"<p><strong>Background: </strong>Venom immunotherapy (VIT) successfully modulates immune responses to venom allergens. However, it may fail in multisensitized patients and cause severe adverse reactions. Bystander suppression mechanisms could enhance VIT efficacy by creating a tolerogenic microenvironment that induces modulatory effects in immune cells, suppressing allergic responses.</p><p><strong>Objective: </strong>This study evaluated the immunomodulatory effect of an oral tolerance induction protocol to ovalbumin (OVA) in an experimental mouse model of allergen sensitization to <i>Polybia paulista</i> (<i>P. paulista</i>) wasp venom.</p><p><strong>Methods: </strong>The humoral immune response was evaluated after the antigen challenge by quantification of specific Immunoglobulin E (sIgE) and mouse mast cell protease 1 (mMcpt1). The functional profiles of splenic dendritic cells and T cells stimulated <i>in vitro</i> with wasp venom allergens or OVA were also analyzed.</p><p><strong>Results: </strong>We observed that oral tolerance induced to OVA modulated the humoral response of previously wasp venom-sensitized mice, reducing the mMcpt1 production but not altering the sIgE to venom allergens of <i>P.paulista</i> wasp. Regarding the cellular response, we observed an increase of tolerogenic DCs and an increased production of IFN-γ, TNF-α, IL-17A and IL-10 cytokines in the cells stimulated with wasp venom allergens. Moreover, there was an increase in the frequency of CD4⁺FoxP3⁺Helios⁺ Treg expressing GARP/LAP markers in comparison with their respective controls.</p><p><strong>Conclusion: </strong>The results suggest that oral tolerance, induced by uncorrelated protein antigen, produces a regulatory immune profile in previously allergen-sensitized mice, which could be exploited to improve the safety and efficacy of AIT protocols, particularly for highly immunogenic allergens.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-11"},"PeriodicalIF":3.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016679","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":"Thioperamide, a histamine H3 receptor antagonist, attenuates neuroimmune activation and inflammation in the SOD1^G93A mouse model of amyotrophic lateral sclerosis.","authors":"Abdullah A Aldossari, Abdulaziz M S Alsaad, Ahmed Nadeem, Mushtaq A Ansari, Sabry M Attia, Saleh A Bakheet, Haneen A Al-Mazroua, Mohammed M Almutairi, Hussain N Alhamami, Wedad S Sarawi, Hatun A Alomar, Majed Ali Algonaiah, Ali A Alshamrani, Alaa A Alanteet, Marwa H Hussein, Mohamed A Mahmoud, Sheikh F Ahmad","doi":"10.1080/08923973.2026.2733883","DOIUrl":"10.1080/08923973.2026.2733883","url":null,"abstract":"<p><strong>Background: </strong>Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder of unknown cause that gradually affects upper and lower motor neurons in the motor cortex, brainstem, and spinal cord. The histamine H3 receptor (H3R), a presynaptic autoreceptor, regulates histamine release through feedback mechanisms. H3R is highly expressed in neurons and microglia, where it influences inflammatory responses.</p><p><strong>Methods: </strong>This study examined the effects of thioperamide, an H3R antagonist, on T cell-mediated immune responses in the SOD1G93A transgenic mouse model of ALS. Mice received daily thioperamide injections (5 mg/kg) for four weeks, beginning at the onset of illness (week 15). Flow cytometry analyzed splenic CD3⁺ T cells for cytokine and marker expression, including IL-1α, IL-6, IFN-γ, TNF-α, IL-17A, RORγt, iNOS, GM-CSF, TGF-β1, and Foxp3. RT-PCR measured mRNA levels in brain tissue.</p><p><strong>Results: </strong>Results showed that thioperamide significantly decreased CD3⁺IL-1α⁺, CD3⁺IL-6⁺, CD3⁺IFN-γ⁺, CD3⁺TNF-α⁺, CD3⁺IL-17A⁺, CD3⁺RORγt⁺, CD3⁺iNOS⁺, and CD3⁺GM-CSF⁺ cells in the spleen, while increasing regulatory CD3⁺TGF-β1⁺ and CD3⁺Foxp3⁺ cells. Similarly, brain tissue showed decreased mRNA levels of IL-1α, IL-6, IFN-γ, TNF-α, IL-17A, RORγt, iNOS, and GM-CSF, with higher TGF-β1 and Foxp3 expression.</p><p><strong>Conclusions: </strong>These findings suggest that thioperamide helps reestablish immune balance in SOD1^G93A mice by influencing both inflammatory and regulatory T cell pathways.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-12"},"PeriodicalIF":3.1,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976922","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":"Statement of Retraction: Anti-inflammatory potential of hecogenin on atopic dermatitis and airway hyper-responsiveness by regulation of pro-inflammatory cytokines.","authors":"","doi":"10.1080/08923973.2026.2732394","DOIUrl":"https://doi.org/10.1080/08923973.2026.2732394","url":null,"abstract":"","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1"},"PeriodicalIF":3.1,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967943","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":"Improvement of post-COVID-19 vaccination dysautonomia with GLP-1 receptor agonist.","authors":"Svetlana Blitshteyn, Jill R Schofield, Nichole Haire, Lawrence B Afrin","doi":"10.1080/08923973.2026.2731357","DOIUrl":"10.1080/08923973.2026.2731357","url":null,"abstract":"<p><strong>Background: </strong>Vasovagal syncope (VVS) is the most common form of cardiovascular dysautonomia that has multiple etiologies. Post-vaccination dysautonomia, in the form of VVS and postural orthostatic tachycardia syndrome, has been reported in the literature after various vaccines, including COVID-19 mRNA vaccination. Treatment of post-vaccination syndromes has not been explored leaving patients with post-vaccination dysautonomia with limited therapeutic options.</p><p><strong>Methods: </strong>We report a 42-year-old woman who developed post-vaccination VVS after COVID-19 mRNA vaccination and improved significantly with semaglutide treatment.</p><p><strong>Results: </strong>The patient's COMPASS-31 score decreased by 44% post-treatment, Orthostatic Hypotension Questionnaire score decreased by 59%, and an average 24-hour heart rate decreased from 97 beats per minute (bpm) to 80 bpm, indicating significant reduction in the autonomic symptom burden. In addition, her post-vaccination neuropathic pain in the legs completely resolved after treatment with semaglutide.</p><p><strong>Conclusion: </strong>This case report suggests that GLP-1 receptor agonists might be beneficial for treatment of recurrent VVS, other forms of dysautonomia and post-vaccination syndromes with neuropathic pain, and may be considered as candidates for randomized placebo-controlled trials in this patient population.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-4"},"PeriodicalIF":3.1,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900478","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":"Targeting TRAF6/MYD88/TLR4, Nrf2, and VEGF signaling pathways by Tranexamic acid as a Novel Therapeutic Approach Protects Against Isotretinoin-Induced Liver Toxicity in Rats.","authors":"Abdullah Alkhammash, Hanan Hagar, Hatem Ali Ahmed Abdelmottaleb, Hamada Hashem, Ghallab Alotaibi, Nervana M K Bayoumy, Deiaa E Elsayed Abouzed","doi":"10.1080/08923973.2026.2733894","DOIUrl":"https://doi.org/10.1080/08923973.2026.2733894","url":null,"abstract":"<p><strong>Background: </strong>Isotretinoin is a widely prescribed retinoid for severe acne but is limited by dose-dependent hepatotoxicity. Tranexamic acid (TXA), an antifibrinolytic agent with emerging anti-inflammatory and antioxidant effects, may offer hepatoprotective potential. Aim: This study evaluated whether TXA mitigates isotretinoin-induced liver injury in rats and explored the underlying molecular mechanisms.</p><p><strong>Methods: </strong>Thirty-two male Wistar rats were assigned to four groups (n = 8 each): control, TXA-only, isotretinoin (ISO, 7.5 mg/kg/day, 30 days), and TXA (100 mg/kg/day for 30 days) + ISO. Serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase were measured for hepatic function. Oxidative stress was assessed by hepatic malondialdehyde, myeloperoxidase (MPO), and reduced glutathione (GSH). Inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin1β (IL-1β), interleukin-10 (IL-10), and signaling proteins TNF receptor-associated factor 6 (TRAF6) and nuclear factor erythroid 2-related factor 2 (Nrf2) were quantified by ELISA. Vascular endothelial growth factor (VEGF) and nuclear factor kappa B (NF-κB) expressions by immunohistochemistry. Myeloid differentiation primary response 88 (MYD88) and toll-like receptor-4 (TLR4) protein expression were analyzed via Western blot. Histopathological scoring was performed to evaluate tissue injury.</p><p><strong>Results: </strong>ISO administration significantly elevated serum ALT and AST by approximately 3-fold (p < 0.001), along with a marked increase in hepatic MDA and MPO, reduced GSH, heightened TNF-α and IL-1β, and suppressed IL-10 (p < 0.05). Hepatic TRAF6, NF-κB, MYD88/TLR4, and VEGF were upregulated significantly (p < 0.05), while Nrf2 was downregulated (p < 0.05), and histology revealed severe degeneration and congestion. TXA co-treatment significantly attenuated these changes (p < 0.05), reducing liver enzyme activities and inflammatory markers while restoring antioxidant defense mechanisms.</p><p><strong>Conclusion: </strong>TXA pretreatment markedly attenuated these effects, normalizing liver enzymes, restoring oxidative balance, reducing inflammation, and suppressing aberrant signaling. TXA effectively protects against isotretinoin-induced hepatotoxicity, primarily through antioxidant and anti-inflammatory mechanisms.</p>","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-18"},"PeriodicalIF":3.1,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967951","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":"Statement of Retraction: Protective effect of Sarsasapogenin in TNBS induced ulcerative colitis in rats associated with downregulation of pro-inflammatory mediators and oxidative stress.","authors":"","doi":"10.1080/08923973.2026.2732397","DOIUrl":"https://doi.org/10.1080/08923973.2026.2732397","url":null,"abstract":"","PeriodicalId":13420,"journal":{"name":"Immunopharmacology and Immunotoxicology","volume":" ","pages":"1-2"},"PeriodicalIF":3.1,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967993","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}