BMC Immunology最新文献

{"title":"High glucose condition aggravates inflammatory response induced by Porphyromonas gingivalis in THP-1 macrophages via autophagy inhibition.","authors":"Yuri Song, Jin-Ju Kwon, Hee Sam Na, Si Yeong Kim, Sang-Hun Shin, Jin Chung","doi":"10.1186/s12865-024-00655-7","DOIUrl":"https://doi.org/10.1186/s12865-024-00655-7","url":null,"abstract":"<p><strong>Background: </strong>Porphyromonase gingivalis (P. gingivalis) is a type of bacteria that causes periodontitis, which is strongly correlated with systemic diseases such as diabetes. However, the effect of hyperglycemia on periodontitis are unclear. The present study examined the effects of high glucose levels on the response to P. gingivalis infection.</p><p><strong>Results: </strong>The expression of P. gingivalis-induced interleukin-1β (IL-1β) and inflammasomes increased as the glucose concentration increased. High glucose conditions suppressed P. gingivalis-induced autophagy in human acute monocytic leukemia cell line (THP-1) macrophages. Zingerone increased autophagy and alleviated P. gingivalis-induced inflammatory response in THP-1 macrophages under high glucose conditions. In addition, P. gingivalis- induced inflammation in bone marrow-derived macrophages of diabetic mice was higher than in wild-type mice, but a zingerone treatment decreased the levels. Alveolar bone loss due to a P. gingivalis infection was significantly higher in diabetic mice than in wild-type mice.</p><p><strong>Conclusions: </strong>High-glucose conditions aggravated the inflammatory response to P. gingivalis infection by suppressing of autophagy, suggesting that autophagy induction could potentially to treat periodontitis in diabetes. Zingerone has potential use as a treatment for periodontal inflammation induced by P. gingivalis in diabetes patients.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"69"},"PeriodicalIF":2.9,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142457636","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":"Regulatory T cells modulate monocyte functions in immunocompetent antiretroviral therapy naive HIV-1 infected people.","authors":"Ambada N Georgia, Ntsama E Claudine, Sake N Carole, Ngu N Loveline, Lissom Abel, Tchouangeu T Flaurent, Sosso Martin, Alain Bopda Waffo, Malachy Okeke, Charles Esimone, Chae Gyu Park, Colizzi Vittorio, Etoa François-Xavier, Nchinda W Godwin","doi":"10.1186/s12865-024-00654-8","DOIUrl":"https://doi.org/10.1186/s12865-024-00654-8","url":null,"abstract":"<p><p>We previously demonstrated that the overall number of regulatory T (Treg) cells decrease proportionately with helper CD4⁺ T cells and their frequencies increase in antiretroviral therapy (ART)-naive human immunodeficiency virus type-1 (HIV-1) infected individuals. The question now is whether the discrepancies in Treg cell numbers and frequencies are synonymous to an impairment of their functions. To address this, we purified Treg cells and assessed their ability to modulate autologous monocytes functions. We observed that Treg cells were able to down modulate autologous monocytes activation as well as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) production during stimulation with polyinosinic-polycytidylic acid stabilized with poly-L-lysine and carboxymethylcellulose (poly-ICLC). This activity of Treg cells has been shown to be influenced by immunocompetence including but not limited to helper CD4⁺ T cell counts, in individuals with HIV-1 infection. Compared to immunosuppressed participants (CD4 < 500 cells/µL), immunocompetent participants (CD4 ≥ 500 cells/µL) showed significantly higher levels of transforming growth factor beta (TGF-β) and IL-10 (p < 0.001 and p < 0.05, respectively), key cytokines used by Treg cells to exert their immunosuppressive functions. Our findings suggest the contribution of both TGF-β and IL-10 in the suppressive activity of Treg cells.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"68"},"PeriodicalIF":2.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11472541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142457637","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":"Correction: Oral Magnesium reduces levels of pathogenic autoantibodies and skin disease in murine lupus.","authors":"Alberto Verlato, Teresina Laragione, Sofia Bin, Randie H Kim, Fadi Salem, Percio S Gulko, Paolo Cravedi","doi":"10.1186/s12865-024-00658-4","DOIUrl":"10.1186/s12865-024-00658-4","url":null,"abstract":"","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"67"},"PeriodicalIF":2.9,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399285","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":"The diagnostic value and validation of IL-22 combimed with sCD40L in tuberculosis pleural effusion.","authors":"Yuzhen Xu, Jing Wu, Qiuju Yao, Qianqian Liu, Huaxin Chen, Bingyan Zhang, Yuanyuan Liu, Sen Wang, Lingyun Shao, Wenhong Zhang, Qinfang Ou, Yan Gao","doi":"10.1186/s12865-024-00652-w","DOIUrl":"10.1186/s12865-024-00652-w","url":null,"abstract":"<p><strong>Background: </strong>There is substantial evidence indicating that cytokines play a role in the immune defense against tuberculosis. This study aims to evaluate the levels of various cytokines in pleural effusion to ditinguish between tuberculosis pleurisy and malignant pleurisy.</p><p><strong>Methods: </strong>A total of 82 participants with pleural effusion were included in the training cohort, and 76 participants were included in the validation cohort. The individuals were divided into tuberculosis and malignant pleurisy groups. The concentrations of interleukin-1β (IL-1β), IL-4, IL-6, IL-10, IL-17 A, IL-17 F, IL-21, IL-22, IL-25, IL-31, IL-33, interferon-γ (IFN-γ), soluble CD40 ligand (sCD40L) and tumor necrosis factor-α (TNF-α) in pleural effusion were measured using a multiplex cytokine assay. The threshold values were calculated according to the receiver operating characteristic (ROC) curve analysis to aid in diagnosing tuberculosis pleurisy. Furthermore, the combined measure was validated in the validation cohort.</p><p><strong>Results: </strong>The levels of all 14 cytokines in pleural effusion were significantly higher in participants with tuberculosis compared to those with malignant pleurisy (all P < 0.05). The area under the curve (AUC) was ≥ 0.920 for the IL-22, sCD40L, IFN-γ, TNF-α and IL-31, which were significantly increased in tuberculous pleural effusion (TPE) compared to MPE in the training cohort. Threshold values of 95.80 pg/mL for IFN-γ, 41.80 pg/mL for IL-31, and 18.87 pg/mL for IL-22 provided ≥ 90% sensitivity and specificity in distinguishing between tuberculosis pleurisy and malignant pleurisy in the training cohort. Among these, IL-22 combined with sCD40L showed the best sensitivity and specificity (94.0% and 96.9%) for diagnosing tuberculosis pleurisy, and this finding was validated in the validation cohort.</p><p><strong>Conclusion: </strong>We demonstrated that the levels of IL-1β, IL-4, IL-6, IL-10, IL-17 A, IL-17 F, IL-21, IL-22, IL-25, IL-31, IL-33, IFN-γ, sCD40L and TNF-α in pleural effusion had significant difference between tuberculosis pleurisy and malignant pleurisy. Specifically, IL-22 ≥ 18.87 pg/mL and sCD40L ≥ 53.08 pg/mL can be clinically utilized as an efficient diagnostic strategy for distinguishing tuberculosis pleurisy from malignant pleurisy.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"66"},"PeriodicalIF":2.9,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11463108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387745","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":"Predictors of change in CD4 cell count over time for HIV/AIDS patients on ART follow-up in northern Ethiopia: a retrospective longitudinal study.","authors":"Gebru Gebremeskel Gebrerufael, Zeytu Gashaw Asfaw","doi":"10.1186/s12865-024-00659-3","DOIUrl":"10.1186/s12865-024-00659-3","url":null,"abstract":"<p><strong>Background: </strong>HIV has an effect on lowering CD4 cell count, which lowers the ability to resist contamination. For patients on ART in areas with limited resources, the CD4 cell count assessment is crucial for determining treatment responses and therapeutic decisions. The volatility of CD4 counts following the introduction of ART over time is still largely uncharacterized, and there are few fresh datasets on CD4 cell count progressions. The goal of this study was to identify the key factors that change over time in CD4 cells for HIV/AIDS patients receiving ART follow-up in northern Ethiopia.</p><p><strong>Methods: </strong>A total of 216 HIV/AIDS patients who initiated ART in the Mekelle General Hospital between 2013 and 2016 were involved using systematic random selection techniques. An examination of exploratory data was used to describe the individual profiles of HIV patients. A multivariable random intercept and slope linear mixed regression analysis regarded predictor variables to be statistically significant if their p-value was less than 0.05.</p><p><strong>Results: </strong>The random intercept and slope linear mixed model result indicated that there were statistically significant predictors of baseline CD4 cell count (β = 0.0125, P-value = 0.001*) and bedridden functional status (β = -2.459, p = 0.02*) on the change of CD4 cell count over time in HIV/AIDS patients at the 5% significance level.</p><p><strong>Conclusions: </strong>Changes in CD4 counts were influenced by the baseline CD4 cell count and the functional status of being bedridden. Because their CD4 cell counts were lower at baseline and they had a functional status of bedridden, the majority of HIV/AIDS patients on ART had substantial predictors on the change of CD4 cell count over time. So, public health service providers should give exceptional guidance and attention is also necessary for those patients who have lower baseline CD4 cell count and bedridden functional status.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"64"},"PeriodicalIF":2.9,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11451158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375057","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":"Correction: Helminth-derived proteins as immune system regulators: a systematic review of their promise in alleviating colitis.","authors":"Maimonah Alghanmi, Faisal Minshawi, Tarfa A Altorki, Ayat Zawawi, Isra Alsaady, Abdallah Y Naser, Hassan Alwafi, Soa'ad M Alsulami, Ala A Azhari, Anwar M Hashem, Rowa Alhabbab","doi":"10.1186/s12865-024-00661-9","DOIUrl":"10.1186/s12865-024-00661-9","url":null,"abstract":"","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"65"},"PeriodicalIF":2.9,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11451257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375056","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":"Inhibition of CEACAM1 expression in cytokine-activated neutrophils using JAK inhibitors.","authors":"Haruki Matsumoto, Ryota Sudo, Yuya Fujita, Michio Onizawa, Kenji Saito, Yuya Sumichika, Shuhei Yoshida, Jumpei Temmoku, Naoki Matsuoka, Tomoyuki Asano, Shuzo Sato, Eiji Suzuki, Takeshi Machida, Kiyoshi Migita","doi":"10.1186/s12865-024-00656-6","DOIUrl":"10.1186/s12865-024-00656-6","url":null,"abstract":"<p><strong>Objectives: </strong>Carcinoembryonic-antigen-related cell-adhesion molecule 1 (CEACAM1) is an adhesion molecule that acts as a coinhibitory receptor in the immune system. We previously demonstrated that CEACAM1 is predominantly expressed on peripheral blood neutrophils in patients with RA. The aim of the present study was to investigate the effects of Janus kinase inhibitors (JAKi) on cytokine-activated human neutrophils and CEACAM1 expression.</p><p><strong>Methods: </strong>Peripheral blood neutrophils were obtained from healthy subjects. Isolated neutrophils were stimulated with tumor necrosis factor-alpha (TNF-α) or granulocyte-macrophage colony-stimulating factor (GM-CSF) in the presence or absence of JAKi. The expression of CEACAM1 in peripheral blood neutrophils was analyzed by flow cytometry. Protein phosphorylation of signal transducer and activator of transcription (STAT)1, STAT3, and STAT5 was assessed by western blot using phospho-specific antibodies.</p><p><strong>Results: </strong>We found that TNF-α-induced CEACAM1 expression was marginally suppressed after pretreatment with pan-JAK inhibitor, tofacitinib. Moreover, TNF-α induced STAT1 and STAT3 phosphorylation at the late stimulation phase (4 to 16 h). The expressions of CEACAM1 on neutrophils were markedly up-regulated by GM-CSF not by interleukin (IL)-6 stimulation. All JAKi inhibited GM-CSF-induced CEACAM1 expressions on neutrophils, however, the inhibitory effects of baricitinib were larger compared to those of tofacitinib or filgotinib. Moreover, CEACAM1 was marginally upregulated in interferon (IFN)-γ stimulated neutrophils. Similarly, JAKi inhibited IFN-γ-induced CEACAM1 expressions on neutrophils.</p><p><strong>Conclusions: </strong>We demonstrated that JAKi prevent GM-CSF-induced CEACAM1 expression in neutrophils, and JAKi-induced inhibition depends on their selectivity against JAK isoforms. These findings suggest that JAKi can modulate the expression of CEACAM1 in cytokine-activated neutrophils, thereby limiting their activation.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"63"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11443749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361055","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":"Autoimmunity's enigmatic role: exploring the connection with myalgic encephalomyelitis/chronic fatigue syndrome.","authors":"Jacob Batham, Jessica Dwyer, Natalie Eaton-Fitch, Sonya Marshall-Gradisnik","doi":"10.1186/s12865-024-00657-5","DOIUrl":"10.1186/s12865-024-00657-5","url":null,"abstract":"<p><strong>Background: </strong>Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complicated, heterogeneous condition distinguished by post-exertional neuroimmune exhaustion and multisystem symptoms. Its complexity poses challenges for physicians, researchers and those inflicted by its presence. Due to conflicting evidence and limiting consensus, the association and contribution autoimmunity serves in the pathophysiology or aetiology of ME/CFS is yet to be confirmed. This systematic review synthesises the currently available data to clarify the role autoimmunity has in the pathogenesis of ME/CFS and explore the therapeutic limitations.</p><p><strong>Methods: </strong>This systematic review was conducted in accordance with the PRISMA and Cochrane guidelines. Full-text articles containing the primary key terms \"Autoimmunity/Autoimmune\" and \"ME/CFS\" were included provided their suitability to the inclusion and exclusion criteria.</p><p><strong>Results: </strong>Ten publications investigating the role of autoimmunity in ME/CFS were examined. One investigated the role of cytokine signalling; Three investigated the genetic nature of autoimmunity in ME/CFS patients; One examined the immune lineage of ME/CFS patients; Six investigated the presence and role of autoantibodies in ME/CFS patients.</p><p><strong>Conclusion: </strong>The findings generated from this systematic review highlight inconsistent and insufficient evidence to classify ME/CFS as an autoimmune disease. Additionally, it further emphasises the complexity of ME/CFS and highlights the challenges in distinguishing autoreactivity from deregulatory processes. Future research is urgently needed to advance the development of diagnostic and treatment strategies.</p><p><strong>Prospero registration code: </strong>CRD42024533447.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"62"},"PeriodicalIF":2.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11443722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361054","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":"Convergence of endothelial dysfunction, inflammation and glucocorticoid resistance in depression-related cardiovascular diseases.","authors":"Zachary Hage, Miguel M Madeira, Dimitris Koliatsis, Stella E Tsirka","doi":"10.1186/s12865-024-00653-9","DOIUrl":"https://doi.org/10.1186/s12865-024-00653-9","url":null,"abstract":"<p><p>Major Depressive Disorder, or depression, has been extensively linked to dysregulated HPA axis function, chronic inflammation and cardiovascular diseases. While the former two have been studied in depth, the mechanistic connection between depression and cardiovascular disease is unclear. As major mediators of vascular homeostasis, vascular pathology and immune activity, endothelial cells represent an important player connecting the diseases. Exaggerated inflammation and glucocorticoid function are important topics to explore in the endothelial response to MDD. Glucocorticoid resistance in several cell types strongly promotes inflammatory signaling and results in worsened severity in many diseases. However, endothelial health and inflammation in chronic stress and depression are rarely considered from the perspective of glucocorticoid signaling and resistance. In this review, we aim to discuss (1) endothelial dysfunction in depression, (2) inflammation in depression, (3) general glucocorticoid resistance in depression and (4) endothelial glucocorticoid resistance in depression co-morbid inflammatory diseases. We will first describe vascular pathology, inflammation and glucocorticoid resistance separately in depression and then describe their potential interactions with one another in depression-relevant diseases. Lastly, we will hypothesize potential mechanisms by which glucocorticoid resistance in endothelial cells may contribute to vascular disease states in depressed people. Overall, endothelial-glucocorticoid signaling may play an important role in connecting depression and vascular pathology and warrants further study.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"25 1","pages":"61"},"PeriodicalIF":2.9,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11428380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142341369","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":"β-glucan combined with Envafolimab and Endostar as immune rechallenge for metastatic non-small cell lung cancer","authors":"Qian Geng, Yingying Lu, Dongqing Li, Lanqun Qin, Chunjian Qi, Xiaolin Pu, Yi Zhuang, Yajun Zhu, Quanbin Zha, Ge Wang, Hua Jiang","doi":"10.1186/s12865-024-00651-x","DOIUrl":"https://doi.org/10.1186/s12865-024-00651-x","url":null,"abstract":"Immune checkpoint inhibitor rechallenge has emerged as a prominent study area in non-small cell lung cancer (NSCLC). β-glucan was reported to reverse resistance to anti-PD-1/PD-L1 inhibitors by regulating the tumor microenvironment. In this self-initiated clinical trial (ChiCTR2100054796), NSCLC participants who have previously failed anti-PD-1 therapy received β-glucan (500 mg, bid, d1-21), Envafolimab (300 mg, d1) and Endostar (210 mg, civ72h) every 3 weeks until disease progression or unacceptable toxicity. The clinical efficacy and adverse events were observed, while serum samples were collected for proteomic analysis. Twenty Three patients were enrolled from January 2022 to March 2023 (median age, 65 years; male, n = 18 [78.3%]; squamous NSCLC, n = 9 [39.1%]; mutant type, n = 13 [56.5%]). The overall response rate (ORR) was 21.7% and disease control rate (DCR) was 73.9%. Median progression-free survival (mPFS) and median overall survival (mOS) was 4.3 months [95% CI: 2.0–6.6] and 9.8 months [95% CI: 7.2–12.4], respectively. The mPFS between PD-L1 positive and negative subgroup has significant difference (6.3 months vs. 2.3 months, p = 0.002). Treatment-related adverse events (TRAEs) occurred in 52.2% of patients. The most common TRAEs were hypothyroidism (26.1%) and fatigue (26.1%). 2 (8.7%) grade 3 adverse events were reported. No adverse reaction related deaths have been observed. Proteomic analysis revealed that the levels of CASP-8, ARG1, MMP12, CD28 and CXCL5 correlated with resistance to the treatment while the levels of CD40-L and EGF related to the favorable response. β-glucan combined with Envafolimab and Endostar has considerable efficacy and safety for immune rechallenge in metastatic NSCLC patients who failed of anti-PD-1 treatment previously, especially for PD-L1 positive patients.","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":"42 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142255014","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}