Kosar M Ali, Nsar Jamal, Shukur Wasman Smail, Martin Lauran, Jonas Bystrom, Christer Janson, Kawa Amin
{"title":"Biomarkers of type 2 and non-type 2 inflammation in asthma exacerbations.","authors":"Kosar M Ali, Nsar Jamal, Shukur Wasman Smail, Martin Lauran, Jonas Bystrom, Christer Janson, Kawa Amin","doi":"10.5114/ceji.2024.141345","DOIUrl":"https://doi.org/10.5114/ceji.2024.141345","url":null,"abstract":"<p><strong>Introduction: </strong>In adult-onset asthma, two major endotypes have been proposed: T2 with eosinophilia and non-T2 characterised by neutrophils and interleukin (IL)-17. The objective of the study was to examine the endotype marker profile in patients with severe asthma who were hospitalized for exacerbations, with a focus on differentiating between viral and non-viral triggers.</p><p><strong>Material and methods: </strong>Forty-nine patients with asthma, admitted for exacerbations, and 51 healthy controls (HCs) were recruited. We further categorized the exacerbated asthma patients into two groups: non-viral infected (n = 38) and viral infected (n = 11) groups. Blood was drawn and a nasopharyngeal swab taken at the time of admission and eosinophil numbers, eosinophil cationic protein (ECP), immuno- globulin E (IgE), tryptase and viral infection were determined. Additionally, levels of IL-17, IL-33 and IL-31 were assessed.</p><p><strong>Results: </strong>The majority of patients had adult onset asthma (age of diagnosis, 42.8 ±16.1) with a duration of 7.7 ±10.8 years, 24.5% being atopic. Patients had higher levels of eosinophils, ECP and IgE than healthy controls (eosinophils, p = 0.003; ECP and IgE, p = 0.0001). Immunohistochemistry confirmed eosinophils as a source of ECP. Tryptase (p = 0.0001), IL-17 (p = 0.0005), IL-31 (p = 0.0001) and IL-33 (p = 0.0002) were also higher in patients than controls. ECP correlated with tryptase (r = 0.08, p = 0.62). IL-17 showed the best correlation with other mediators, including ECP (r = 0.35, p = 0.24), tryptase (r = 0.69, p = 0.0001), IgE (r = 0.50, p = 0.0001), IL-33 (r = 0.95, p = 0.0001) and IL-31 (r = 0.89, p = 0.0001). IgE, IL-17, and IL-31 had a high AUC when differentiating those with severe and non-severe asthma. The group with exacerbated viral infection showed elevated levels of serum IL-17 and IL-31 compared to the non-infected group.</p><p><strong>Conclusions: </strong>Patients with asthmatic exacerbations were found to have higher levels of both T2 and non-T2 inflammatory markers than healthy controls. In the study, levels of IgE, IL-17, and IL-31 differentiated between patients with severe and non-severe asthma. The last two cytokines were also able to distinguish between exacerbated asthma caused by viral infection and exacerbated asthma caused by non-viral infection.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"49 2","pages":"203-213"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388339","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 N6-methyladenosine pattern of MAP3K7 mediates the effects of sevoflurane on macrophage M2 polarization and cervical cancer migration and invasion.","authors":"Luxin Huang, Feng Duan, Xianning Dong, Zengzhen Zhang","doi":"10.5114/ceji.2024.145307","DOIUrl":"10.5114/ceji.2024.145307","url":null,"abstract":"<p><strong>Introduction: </strong>The study was designed to determine whether and how sevoflurane (Sev) regulates tumor associated macrophage (TAM) polarization and cervical cancer (CC) cell progression.</p><p><strong>Material and methods: </strong>The M2 polarized THP-1 was treated with 3%Sev. The culture supernatant of M2 polarized THP-1 was co-cultured with the CC cell line Hela. The NF-<i>κ</i>B activity was determined by luciferase reporter assay. The key genes dis-regulated by 3%Sev were determined by RNA sequencing (RNA-seq) followed by real-time reverse transcription PCR (qRT-PCR) assay. Luciferase reporter assay was used to analyze the function of 3%Sev based on N6-methyladenosine (m6A) site activity on MAP3K7 3 <i>'</i> untranslated regions (3 <i>'</i> UTRs). RNA immunoprecipitation (IP) using an anti-m6A antibody (anti-m6A RNA-IP) was performed to determine the m6A levels at MAP3K7 3 <i>'</i> UTR.</p><p><strong>Results: </strong>3%Sev treatment significantly up-regulated the M2 polarization markers and down-regulated the NF-<i>κ</i>B activity of THP-1. Meanwhile, 3%Sev treated macrophages could enhance the migratory and invasive potential of CC cells. Further, 3%Sev significantly regulated the NF-<i>κ</i>B pathway, including MAP3K7 inhibition. MAP3K7 overexpression reversed the 3%Sev-regulated NF-<i>κ</i>B activity and M2 polarization. 3%Sev treatment increased m6A levels in the 3 <i>'</i> UTR of MAP3K7. Mutational analysis of potential m6A sites within MAP3K7 3 <i>'</i> UTR revealed that these sites were required for 3%Sev regulation. In conclusion, the m6A pattern of MAP3K7 mediates the effects of 3%Sev on macrophage M2 polarization and cervical cancer progression.</p><p><strong>Conclusions: </strong>3%Sev enhanced TAMs M2 polarization through regulating the m6A pattern of MAP3K7, and therefore enhanced the stimulatory effect of M2 TAMs on the migration and invasion of CC cells.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"49 4","pages":"393-403"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11811724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406075","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}
Jingyi Li, Gang Zhou, Te Chen, Qiao Lin, Qiupeng Yang
{"title":"LncRNA RMRP promotes chondrocyte injury by regulating the FOXC1/RBP4 axis.","authors":"Jingyi Li, Gang Zhou, Te Chen, Qiao Lin, Qiupeng Yang","doi":"10.5114/ceji.2024.145312","DOIUrl":"10.5114/ceji.2024.145312","url":null,"abstract":"<p><strong>Introduction: </strong>The main pathological feature of osteoarthritis (OA) is chondrocyte injury. LncRNA mitochondrial RNA processing endoribonuclease (RMRP) has been shown to be a chondrogenic differentiation factor. This study aimed to explore the role of RMRP in chondrocyte injury.</p><p><strong>Material and methods: </strong>Cell counting kit-8 (CCK-8) and TUNEL assays were used to determine lipopolysaccharide (LPS)-induced chondrocyte viability and apoptosis, respectively. The interaction between RMRP and FOXC1 was analyzed by RIP and RNA pull-down. Dual luciferase reporter and ChIP were employed to analyze the interaction between FOXC1 and RBP4. The levels of RMRP, FOXC1, RBP4, apoptosis-related and extracellular matrix (ECM)-related genes were detected by RT-qPCR and western blot. ELISA assay was used for detection of inflammatory cytokines in LPS-induced chondrocytes.</p><p><strong>Results: </strong>The levels of RMRP, FOXC1 and RBP4 were significantly upregulated in OA cartilage tissues and LPS-induced chondrocytes. Knockdown of RMRP inhibited chondrocyte apoptosis and inflammation under LPS. RMRP interacted with FOXC1 and promoted RBP4 expression. FOXC1 could upregulate RBP4 and promote LPS-induced chondrocyte apoptosis and inflammation. Similarly, RMRP combined with FOXC1 and aggravated apoptosis and inflammation in LPS-treated chondrocytes.</p><p><strong>Conclusions: </strong>RMRP promoted upregulation of RBP4 and activation of the JNK signaling pathway by binding to FOXC1, thereby accelerating LPS-induced apoptosis and inflammation in chondrocytes.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"49 4","pages":"366-382"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11811726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406093","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}
Eliza Glodkowska-Mrowka, Marlena Tynecka, Andrzej Eljaszewicz
{"title":"How BATF silencing protects neonatal lungs in sepsis.","authors":"Eliza Glodkowska-Mrowka, Marlena Tynecka, Andrzej Eljaszewicz","doi":"10.5114/ceji.2024.145408","DOIUrl":"10.5114/ceji.2024.145408","url":null,"abstract":"","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"49 3","pages":"215"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885004","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":"STK11 mutation affects tumor proliferation by impacting CD4<sup>+</sup> T cell activity in lung adenocarcinoma.","authors":"Jiemeng Ge, Rui Feng, Feihu Zhu, Zhihui Xu, Qiangwei Chi, Zhenye Lv","doi":"10.5114/ceji.2024.143578","DOIUrl":"10.5114/ceji.2024.143578","url":null,"abstract":"<p><strong>Introduction: </strong>STK11 mutation is common in lung adenocarcinoma (LUAD), but the molecular mechanism of STK11 regulation in LUAD remains uncharacterized. This study intended to explore the effect of STK11 mutation on activity and proliferation of CD4<sup>+</sup> T cells in LUAD.</p><p><strong>Material and methods: </strong>qRT-PCR experiments verified the STK11 level in different cell models. Cell Counting Kit-8 (CCK-8) and colony formation experiments evaluated proliferation ability. CCK-8 detected activity of CD4<sup>+</sup> T cells. Immunohistochemistry detected levels of related genes. Immunofluorescence assayed levels of CD4<sup>+</sup> T cell infiltration.</p><p><strong>Results: </strong>STK11 mutation could accelerate proliferation of LUAD cells and impact activity of CD4<sup>+</sup> T cells. Further research found that STK11 mutation affected tumor proliferation by impacting CD4<sup>+</sup> T cell activity in LUAD.</p><p><strong>Conclusions: </strong>This study revealed the regulatory mechanism of STK11 mutation affecting tumor proliferation by impacting CD4<sup>+</sup> T cell activity in LUAD. It suggested that STK11 may be a possible biological target for LUAD patients, and inhibiting STK11 mutation or cutting off its regulatory pathway for immune function may be an effective strategy for STK11-mutated tumor patients.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"49 3","pages":"320-330"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885057","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}
Mateusz P. Łyżwa, Karolina Kędziora, Natalia Kałamarz, Jowita Frączkiewicz, Anna Panasiuk, Joanna Owoc-Lempach, Barbara Piątosa, Marcin Hennig, Ninela Irga-Jaworska, Krzysztof Kałwak
{"title":"Hematopoietic stem cell transplantation in a patient with activated phosphoinositide 3‑kinase δ syndrome: A case report and literature review","authors":"Mateusz P. Łyżwa, Karolina Kędziora, Natalia Kałamarz, Jowita Frączkiewicz, Anna Panasiuk, Joanna Owoc-Lempach, Barbara Piątosa, Marcin Hennig, Ninela Irga-Jaworska, Krzysztof Kałwak","doi":"10.5114/ceji.2023.133949","DOIUrl":"https://doi.org/10.5114/ceji.2023.133949","url":null,"abstract":"Activated phosphoinositide 3-kinase δ syndrome (APDS) is a recently described disease characterized by recurrent infections, lymphoproliferation with a high risk of malignancy, early-onset cytopenia, and a propensity for autoimmune diseases. Hematopoietic stem cell transplantation (HSCT) has proven to be an effective treatment method; however, the recovery process after HSCT is prolonged and accompanied by complications. In this study, we present the case of a patient with APDS type 1. Despite showing signs of immunodeficiency at the age of 6 months, it took almost 6 years to reach a definitive diagnosis. The patient experienced recurrent infections, often accompanied by anemia requiring transfusions, and multifocal nonmalignant lymphoproliferation. Only after receiving the appropriate diagnosis was it possible to implement proper and accurate treatment. HSCT was performed when the patient was 6 years old, leading to significant improvement in his condition. At the 17-month post-HSCT follow-up, the boy is asymptomatic and in good general health, although close monitoring continues due to mixed chimerism and delayed humoral immune recovery. Applying HSCT before the patient develops malignancy contributes to expanding the use of HSCT as a treatment option for APDS type 1.","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"12 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139910742","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":"The role of inflammatory and remodelling biomarkers in patients with non-small cell lung cancer","authors":"Hemn Abdalla Omer, Christer Janson, Kawa Amin","doi":"10.5114/ceji.2023.133725","DOIUrl":"https://doi.org/10.5114/ceji.2023.133725","url":null,"abstract":"<b>Introduction:</b><br/>Biomarkers play a crucial role in evaluating the prognosis, diagnosis, and monitoring of non-small cell lung cancer (NSCLC). The aim of this study was to compare the levels of inflammatory and remodelling biomarkers among patients with NSCLC and healthy controls (HCs) and to investigate the correlation between these biomarkers.<br/><br/><b>Material and methods:</b><br/>Blood samples were taken from 93 NSCLC and 84 HCs. Each sample was analysed for the inflammatory biomarkers transforming growth factor β1 (TGF-β1), mothers against decapentaplegic homolog 2 (SMAD2) and the remodelling biomarkers Wingless-related integration site (Wnt3a) and β-catenin (CTNN-β1).<br/><br/><b>Results:</b><br/>The patients with NSCLC had significantly higher levels of all the measured biomarkers. In the NSCLC patients, TGF-β1 correlated significantly with SMAD2 (<i>r</i> = 0.34, <i>p</i> = 0.0008), Wnt3a (<i>r</i> = 0.328, <i>p</i> = 0.0013), and CTNN-β1 levels (<i>r</i> = 0.30, <i>p</i> = 0.004). SMAD2 correlated significantly with CTNN β1 (<i>r</i> = 0.546, <i>p</i> = 0.0001) and Wnt3a (<i>r</i> = 0.598, <i>p</i> = 0.0001). CTNN-β1 level also correlated with the level of Wnt3a (<i>r</i> = 0.61, <i>p</i> = 0.0001). No correlation was found between biomarkers and symptom scores.<br/><br/><b>Discussion:</b><br/>In this study, patients with NSCLC had higher inflammatory and remodelling biomarker levels than HCs. In the NSCLC, there were significant associations between inflammatory and remodelling biomarkers. This indicates that measuring biomarkers could be valuable in the workup of NSCLC patients.<br/><br/><b>Conclusions:</b><br/>Our investigation showed that inflammatory and remodelling biomarkers might play a role in future immunologic response and pharmacologically targeted NSCLC therapy.<br/><br/>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"69 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139924137","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}
Ieva Vanaga, Oksana Kolesova, Aleksandrs Kolesovs, Gunta Sture, Elvira Hagina, Jelena Storozenko, Liene Nikitina-Zake, Ludmila Viksna
{"title":"Association of human leukocyte antigen class II alleles with epithelial cell apoptosis and extracellular matrix production in acute COVID-19","authors":"Ieva Vanaga, Oksana Kolesova, Aleksandrs Kolesovs, Gunta Sture, Elvira Hagina, Jelena Storozenko, Liene Nikitina-Zake, Ludmila Viksna","doi":"10.5114/ceji.2023.133684","DOIUrl":"https://doi.org/10.5114/ceji.2023.133684","url":null,"abstract":"<b>Introduction:</b><br/>Pathogenic mechanisms and long-term consequences of COVID-19 require attention in studies on SARS-CoV-2. The association of the severity of COVID-19 with genetic factors, such as human leukocyte antigen (HLA) genes, remains underexplored. Our study assessed the relationships between HLA class II alleles and COVID-19 severity and blood-based indicators of systemic inflammation and organ damage, serum markers of epithelial cell apoptosis such as caspase-cleaved CK18 fragment M30 (CK18-M30) and the extracellular matrix product hyaluronic acid (HA).<br/><br/><b>Material and methods:</b><br/>The study included 101 hospitalized COVID-19 patients (mean age 60 ±14 years). Clinical tests were performed at admission to the hospital. The levels of CK18-M30 and HA were detected in serum by enzyme-linked immunosorbent assay (ELISA). HLA typing was performed in HLA-DRB1, -DQA1, and -DQB1 loci by the polymerase chain reaction with low-resolution sequence-specific primers.<br/><br/><b>Results:</b><br/>Sixty-one patients had a non-severe and 40 had a severe or critical disease course (following the WHO definition). The severity was associated with older age, male gender, higher HA, CK18-M30, and some indicators of inflammation. Despite the lack of direct association between HLA alleles and the severity of COVID-19, the presence of HLA-DRB1*04 and 12 alleles in the genotype was associated with lowered or elevated HA, respectively. The HLA-DQB1*03:01 allele was associated with lowered CK18-M30, aspartate aminotransferase, and ferritin. In addition, HLA-DQB1*06:01 was associated with elevated alanine aminotransferase.<br/><br/><b>Conclusions:</b><br/>Associations of HLA class II alleles with markers of epithelial cell apoptosis and extracellular matrix production indirectly support the influence of HLA genes on acute COVID-19 severity.<br/><br/>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"2 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139923883","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}
Jaroslaw Nowakowski, Anna Tomoń, Dorota Telesińska-Jasiówka
{"title":"Newly diagnosed seropositive rheumatoid arthritis in a 52-year-old man superimposed on long-standing ankylosing spondylitis during secukinumab treatment","authors":"Jaroslaw Nowakowski, Anna Tomoń, Dorota Telesińska-Jasiówka","doi":"10.5114/ceji.2023.132066","DOIUrl":"https://doi.org/10.5114/ceji.2023.132066","url":null,"abstract":"rheumatoid arthritis (ra) and ankylosing spondylitis (as) are severe chronic inflammatory joint diseases with different immune-mediated mechanisms playing a role in their pathogenesis. rheumatoid arthritis is an erosive arthritis of peripheral joints and as is a spondyloarthropathy affecting mainly sacroiliac and spinal joints leading to excessive bone formation and ankylosis. The coexistence of rA and As in the same patient is rare. Presented here is a 52-year-old patient with long-standing As with bilateral ankylosis of sacroiliac joints who developed peripheral symmetric polyarthritis while being treated with the interleukin 17 inhibitor secukinumab introduced due to secondary inefficacy of the tu - mor necrosis a inhibitor etanercept. He was finally diagnosed with seropositive rA coexisting with As and treatment was changed to the Janus kinase inhibitor tofacitinib. eventually, remission was sustained with use of the interleukin 6 inhibitor tocilizumab. This is the first case of rA developing during anti-interleukin 17 therapy. Although tocilizumab lacks efficaciousness in As, in this case therapy was succesful as the rA-driving cytokine mechanism possibly prevailed.","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"41 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135059027","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":"Immunotherapy of B cell lymphoma with CD22-redirected CAR NK-92 cells.","authors":"Xiaopeng Tian, Ruixi Zhang, Huimin Qin, Xiangru Shi, Wenhui Qi, Dongpeng Jiang, Tingting Zhu, Aining Sun","doi":"10.5114/ceji.2023.126672","DOIUrl":"https://doi.org/10.5114/ceji.2023.126672","url":null,"abstract":"<p><strong>Introduction: </strong>Chimeric antigen receptor (CAR)-NK cells are considered safer than CAR-T cells due to their short lifetime and production of lower toxicity cytokines. By virtue of unlimited proliferative ability in vitro, NK-92 cells could be utilized as the source for CAR-engineered NK cells. CD22 is highly expressed in B cell lymphoma. The goal of our study was to determine whether CD22 could become an alternative target for CAR-NK-92 therapy against B cell lymphoma.</p><p><strong>Material and methods: </strong>We first generated m971-BBZ NK-92 that expressed a CAR for binding CD22 in vitro. The expression of CAR was assessed by flow cytometric analysis as well as immunoblotting. The cytotoxicity of the m971-BBZ NK-92 cells towards target lymphoma cells was determined by the luciferase-based cytolysis assay. The production of cytokines in CAR NK-92 cells in response to target cells was evaluated by ELISA assay. Lastly, the cytolytic effect was evaluated by the cytolysis assay mentioned above following irradiation. The level of inhibitory receptor of CAR-expressing cells was assessed by flow cytometry.</p><p><strong>Results: </strong>CD22-specific CAR was expressed on m971-BBZ NK-92 cells successfully. m971-BBZ NK-92 cells efficiently lysed CD22-expressing lymphoma cells and produced large amounts of cytokines after coculture with target cells. Meanwhile, irradiation did not apparently influence the cytotoxicity of m971-BBZ NK-92 cells. Inhibitory receptor detection exhibited a lower level of PD-1 in m971-BBZ NK-92 cells than FMC-63 BBZ T cells after repeated antigen stimulation.</p><p><strong>Conclusions: </strong>Our data show that adoptive transfer of m971-BBZ NK-92 could serve as a promising strategy for immunotherapy of B cell lymphoma.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"48 1","pages":"1-13"},"PeriodicalIF":1.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/17/d1/CEJI-48-50550.PMC10189576.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9930543","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}