Immunobiology最新文献

{"title":"Mannose receptor modulates hepatic stellate cell activation and alleviates liver fibrosis through immune-fibrotic crosstalk","authors":"Shiyue Tang,&nbsp;Shengnan Luo,&nbsp;Jun Zhang,&nbsp;Dehe Zhang,&nbsp;Xiaoping Wang,&nbsp;Haijun Chen","doi":"10.1016/j.imbio.2026.153189","DOIUrl":"10.1016/j.imbio.2026.153189","url":null,"abstract":"<div><h3>Background</h3><div>Liver fibrosis is characterized by excessive extracellular matrix (ECM) deposition and hepatocellular dysfunction. Activation of hepatic stellate cells (HSCs) is central to this process, yet the underlying regulatory mechanisms remain incompletely understood. The mannose receptor (MR), a pattern-recognition receptor involved in immune modulation and tissue remodeling, has been implicated in fibrotic diseases, but its role in hepatic fibrosis remains unclear.</div></div><div><h3>Methods</h3><div>A chronic liver fibrosis model was established in mice using repeated carbon tetrachloride (CCl₄) injection. Histology, serum biochemistry, quantitative PCR, and Western blotting were used to evaluate fibrosis, HSC activation, and MR expression. Correlations between MR and inflammatory cytokines were analyzed. In vitro, MR overexpression was used to assess its role in transforming growth factor-β (TGF-β)-induced HSC activation.</div></div><div><h3>Results</h3><div>CCl₄-induced fibrosis resulted in hepatocyte injury, ECM accumulation, and elevated ALT, AST, and triglyceride levels. HSC activation, indicated by increased α-SMA and collagen I expression, accompanied fibrosis progression. MR expression in liver tissue and soluble MR (sMR) levels in serum were significantly increased and were associated with inflammatory cytokines. In vitro, MR overexpression suppressed TGF-β–induced HSC activation without altering total Smad-3 expression.</div></div><div><h3>Conclusion</h3><div>These findings suggest that MR may play a regulatory role in hepatic fibrogenesis by modulating HSC activation and ECM deposition, potentially through interactions with the inflammatory microenvironment. Elevated MR and sMR levels may serve as candidate biomarkers for fibrosis progression.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 3","pages":"Article 153189"},"PeriodicalIF":2.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147850199","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":"Factor H-related proteins as a protective evolutionary mechanism against microbial infections","authors":"Rosario García-Sánchez ,&nbsp;Alberto López-Lera ,&nbsp;Laura González-Sánchez ,&nbsp;Fernando Corvillo ,&nbsp;Agustín Tortajada ,&nbsp;Pilar Sánchez-Corral","doi":"10.1016/j.imbio.2026.153185","DOIUrl":"10.1016/j.imbio.2026.153185","url":null,"abstract":"<div><div>Factor H (FH) is the main regulator of the complement alternative pathway, and it is essential to prevent complement-mediated autologous damage. Many pathogens express FH-binding proteins on their surface that recruit human FH as a strategy to avoid or limit their elimination by the host complement. The FH-Related Proteins (FHR-1, FHR-2, FHR-3, FHR-4A, and FHR-5) share sequential and structural homology with FH that result from their common ancestry, but none of them can regulate complement like FH. While the precise contribution of FHRs in human complement is still not completely understood, it has been proposed that these proteins have been conserved along evolution because they outcompete FH binding to the microbial surfaces, thus allowing pathogen elimination. In this review, we recapitulate the current evidence of the interaction between FHRs and pathogens. We describe the results from “in vitro” studies with microbial isolates and purified proteins, and the few studies that have addressed the quantification of FH and FHRs in patients during infection. We also provide an analysis comparing the frequency of common genetic variants, including <em>ΔCFHR3-CFHR1,</em> in different geographical regions, and the incidence of Invasive Meningococcal Disease. All the data are discussed in the context of the role of FHRs as FH-deregulators, and at the light of recent findings supporting a function as complement activators.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 3","pages":"Article 153185"},"PeriodicalIF":2.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147850776","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":"Complement in tuberculosis infection and disease, a battle of two ancients","authors":"Karin Dijkman ,&nbsp;Simone A. Joosten ,&nbsp;Leendert A. Trouw","doi":"10.1016/j.imbio.2026.153183","DOIUrl":"10.1016/j.imbio.2026.153183","url":null,"abstract":"<div><div>Tuberculosis continues to kill over a million people every year, with an additional 10 million people falling ill. The ongoing efforts to eradicate the disease are hampered by an incomplete understanding of the mechanisms involved in the defense against tuberculosis. It has become clear that next to the well-known T-cell responses other components of the immune system also play important roles, both protective and detrimental, in the host defense against tuberculosis. In particular, the role of antibodies and complement are increasingly appreciated. However, the contribution of the complement system during <em>Mycobacterium tuberculosis</em> infection and disease remains poorly understood. The complement system is an intricate network of plasma proteins, which upon activation can achieve a powerful cytotoxic effect. Additionally, a range of antimicrobial and immune-modulating effector molecules, such as opsonins and chemoattractants, are generated. As a consequence, the role of the complement system in host defense extends beyond its cytotoxic effect, influencing both the innate and adaptive immune response. In this review, we discuss the many-faceted role of the complement system in tuberculosis, reviewing its involvement in infection, disease progression, and response to therapy, and provide a perspective on how the complement system can be harnessed to improve tuberculosis diagnostics, vaccines and therapeutics.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 3","pages":"Article 153183"},"PeriodicalIF":2.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147798644","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":"Blue light-emitting diode phototherapy reduces cerebral parasitic load and inflammation in murine congenital toxoplasmosis model","authors":"Débora Nonato Miranda Toledo ,&nbsp;Natiele Carlos ,&nbsp;Giulia Caroline Dantas-Vieira ,&nbsp;Marina Monteiro de Castro Burle ,&nbsp;Lauro de Assis Duarte-Junior ,&nbsp;Maria Laura Cruz Castro ,&nbsp;Talita Rodrigues dos Santos ,&nbsp;Guilherme Paula Costa ,&nbsp;Cristiano Schetini de Azevedo ,&nbsp;Daniela Caldeira Costa ,&nbsp;Élida Mara Leite Rabelo ,&nbsp;Rodrigo Fernando Bianchi ,&nbsp;Érica Santos Martins-Duarte ,&nbsp;André Talvani","doi":"10.1016/j.imbio.2026.153182","DOIUrl":"10.1016/j.imbio.2026.153182","url":null,"abstract":"<div><div>The search for effective therapies to eradicate <em>Toxoplasma gondii</em>, the causative agent of toxoplasmosis, has spanned decades with limited success. Current drugs, including sulfadiazine, spiramycin, and pyrimethamine, face limitations such as parasite resistance, high cellular toxicity, inconsistent efficacy in the acute phase of disease, and the lack of effect in the chronic phase. This study evaluates an innovative adjunctive approach using light-emitting diode phototherapy (BLP) to control <em>T. gondii</em> acute infection during pregnancy. For that, pregnant female Swiss mice (8–9 weeks) were orally infected with 10 cysts of the ME49 strain of <em>T. gondii</em> and exposed to BLP (460 nm, 7 μW/cm2) or conventional white light for 12 h/day over 12 days. After the treatment period, the females were euthanized, and the fetuses, placentas, liver, spleen, maternal brain, and blood were collected for analysis. BLP reduced parasitic load in brain tissue and modulated tissue-specific immune responses, with increased IL-10 in the brain and fetal tissues, elevated CCL2 in liver parenchyma and fetal tissues, and induction of TNF in fetal samples. Serum ferritin and oxidative stress, thiobarbituric acid-reactive substances (TBARS), and superoxide dismutase (SOD) increased in infected mice exposed to BLP, while catalase (CAT) remained unchanged. These findings suggest that BLP exerts both immunomodulatory effects on the infected host and cytotoxicity against <em>T. gondii</em>, supporting its potential as an adjunctive approach for etiological treatment in congenital toxoplasmosis.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 3","pages":"Article 153182"},"PeriodicalIF":2.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837418","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":"Estrogen ameliorates Caerulein-induced inflammatory injuries and oxidative stress in acute pancreatitis via STAT3/PGAM1 signaling","authors":"Weixi Shan,&nbsp;Wenyu Zhou,&nbsp;Ya Huang,&nbsp;Hengyang Ou,&nbsp;Long Yang","doi":"10.1016/j.imbio.2026.153177","DOIUrl":"10.1016/j.imbio.2026.153177","url":null,"abstract":"<div><h3>Background</h3><div>Acute pancreatitis (AP) is an acute inflammatory abdominal disease frequently associated with intestinal barrier dysfunction. The steroid hormone 17β-estradiol is an estrogen that exhibits anti-inflammatory effects in various inflammatory diseases. However, its potential beneficial effects on AP and the underlying mechanism have not been investigated.</div></div><div><h3>Methods</h3><div>57 patients with AP and 30 healthy volunteers were enrolled in this study. Caerulein-induced human pancreatic duct epithelial (HPDE) cells were used to establish an in vitro research model. Phosphoglycerate mutase 1 (PGAM1) and Signal transducer and activator of transcription 3 (STAT3) were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot. Tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 levels were analyzed using ELISA kits and RT-qPCR assay. Reactive oxygen species (ROS), malondialdehyde (MDA), Superoxide dismutase (SOD), and Catalase (CAT) products were detected using special assay kits. Following JASPAR prediction, the binding between STAT3 and the PGAM1 promoter was verified using Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. The effects of 17β-estradiol, STAT3, and PGAM1 on Caerulein-induced HPDE cell damage were assessed. The impacts of 17β-estradiol and STAT3 on pancreatic injury in Caerulein-induced AP mouse model.</div></div><div><h3>Results</h3><div>PGAM1 and STAT3 were highly expressed in AP patients and Caerulein-treated HPDE cells. PGAM1 silencing alleviated Caerulein-triggered HPDE cell inflammatory injury and oxidative stress. Mechanistically, STAT3 was a transcription factor of PGAM1 that promoted PGAM1 transcription by directly binding to its promoter region. 17β-estradiol repressed Caerulein-caused HPDE cell inflammatory injury and oxidative stress by regulating the STAT3/PGAM1. In addition, 17β-estradiol treatment attenuated pancreatic injury in cerulein-induced AP mice by regulating STAT3.</div></div><div><h3>Conclusion</h3><div>17β-estradiol treatment blocked Caerulein-induced HPDE cell inflammatory injury and oxidative stress by targeting the STAT3/PGAM1 axis, providing a promising strategy to protect against AP.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 3","pages":"Article 153177"},"PeriodicalIF":2.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770166","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":"Cell-free supernatant of Clostridium butyricum induces mitochondrial apoptosis and suppresses NF-κB pathway in colorectal cancer cells","authors":"Miao Liu ,&nbsp;Shuping Liu ,&nbsp;Wenjie Xie ,&nbsp;Guang Li ,&nbsp;Tao Deng","doi":"10.1016/j.imbio.2026.153172","DOIUrl":"10.1016/j.imbio.2026.153172","url":null,"abstract":"<div><h3>Background</h3><div><em>Clostridium butyricum</em> (CB), a butyrate-producing probiotic, exhibits antitumor potential in colorectal cancer (CRC). This study investigated the direct effects and mechanisms of CB-secreted metabolites on CRC cells.</div></div><div><h3>Methods</h3><div>HT-29 cells were treated with serial dilutions (5–40%) of sterile-filtered CB supernatant (CBS), using <em>E. coli</em> DH5α supernatant as control. Cell viability and proliferation were assessed by CCK-8 and Ki-67 immunofluorescence. Apoptosis was evaluated by Annexin V/PI flow cytometry. Mitochondrial membrane potential (ΔΨm) was monitored via JC-1 staining. Apoptosis-related and NF-κB pathway proteins were analyzed by Western blot.</div></div><div><h3>Results</h3><div>The CBS notably suppressed HT-29 cell viability and proliferation as concentration and treatment duration increased, with an IC₅₀ of 18.84% (95% CI: 16.2% to 21.5%) at 48 h. CBS exposure markedly increased apoptotic cell proportion. Mechanistically, CBS induced ΔΨm loss, cytosolic cytochrome <em>c</em> translocation, and activation of caspase-9 and -3. Concurrently, CBS inhibited NF-κB pathway activation, downregulated Bcl-2, and upregulated Bax.</div></div><div><h3>Conclusion</h3><div>CB culture supernatant inhibits growth and induces apoptosis in HT-29 cells through mitochondrial dysfunction and NF-κB suppression.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153172"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147448670","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":"Programmed death-ligand 1 correlates with acute influenza B virus infection","authors":"Hong Zhang ,&nbsp;Ming Liu ,&nbsp;Tongbao Feng ,&nbsp;Ping Zhang ,&nbsp;Yan Wang","doi":"10.1016/j.imbio.2026.153165","DOIUrl":"10.1016/j.imbio.2026.153165","url":null,"abstract":"<div><div>Programmed Death-Ligand 1 (PD-L1) has been proven to mediate various mechanisms to induce T-cell dysfunction in influenza A virus infection. However, whether PD-L1 similarly contributes to inflammatory responses during influenza B virus (IBV) infection remains unknown. Here we investigated PD-L1 expression patterns during acute IBV infection. A total of 24 IBV-infected patients and 33 healthy controls were recruited and assigned to three age subgroups. Using flow cytometry, we assessed PD-L1 expression on circulating leukocytes and measured the concentrations of plasma cytokines. Our findings demonstrated that IBV infection induced PD-L1 expression on human dendritic cells, T-cells and monocytes. Additionally, IL-2, IL-4, IL-6, IL-10, and TNF concentrations elevated significantly, indicating the occurrence of robust inflammatory responses. Notably, age did not influence PD-L1 expression on peripheral immune cells across the three age subgroups. These results reveal that IBV infection involves the expression of PD-L1 on key immune cell populations, and PD-L1 may serve as a target in the design of new therapeutic strategies for IBV.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153165"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147270833","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":"Differential astrocyte activation by Taenia solium antigens: Specific induction of IL-10 and IL-1β by Excretory/Secretory (ES) products","authors":"Kevin Gonzales,&nbsp;Jessy Condori,&nbsp;Guillermo Fernández ,&nbsp;Manuela Verastegui","doi":"10.1016/j.imbio.2026.153162","DOIUrl":"10.1016/j.imbio.2026.153162","url":null,"abstract":"<div><div><strong>Background:</strong> Neurocysticercosis (NCC) is a parasitic infection of the central nervous system (CNS) caused by the larval form of <em>Taenia solium</em>. This disease provokes an inflammatory response that intensifies when the parasite dies. This study aimed to assess the expression of the cytokines IL-10, IL-1β, and TGF-β in primary astrocyte cultures derived from rat brains at 5 and 14 days in vitro (DIV) following exposure to <em>T. solium</em> cysticercus antigens. <strong>Methods:</strong> Primary astrocyte cultures obtained from 3-day-old postnatal rats were incubated for 24 h with either Excretory/Secretory (E/S) antigens or Total antigen (Tag), while lipopolysaccharide (LPS) was used as a positive control. Cytokine expression (IL-10, IL-1β, and TGF-β1) was quantified by RT-qPCR. <strong>Results:</strong> DIV5 culture contains astrocytes and neurons, while in DIV14 only astrocytes were detected. At DIV5, the incubation with E/S products increased the gene expression of IL-10 and IL-1β. Conversely,at DIV14, E/S antigens only augmented IL-10 mRNA levels. Moreover, Tag did not change IL-10, IL-1β, and TGF-β gene expression in both DIV5 and DIV14 cultures. Finally, TGF-β expression remains unchanged after <em>T. solium</em> antigen exposure. <strong>Conclusions:</strong> <em>T. solium</em> E/S products may differentially modulate astrocyte cytokine responses in a stage-dependent manner. In addition, the Tag obtained from viable cysts does not affect the studied cytokine gene expression. These results underscore the potential role of astrocytes in the neuroinflammatory processes associated with NCC.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153162"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118886","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":"Unmodified γδ T cells exhibit potent antitumor activity in hepatocellular carcinoma and are enhanced by PD-L1 blockade","authors":"Bo-Xiang Benjamin Zhang ,&nbsp;Hong-Yi Lin ,&nbsp;Hoang Yen Tran ,&nbsp;Chung-Che Wu ,&nbsp;Kai-Yun Chen ,&nbsp;Tsung-I Hsu ,&nbsp;Chih-Jie Shen","doi":"10.1016/j.imbio.2026.153163","DOIUrl":"10.1016/j.imbio.2026.153163","url":null,"abstract":"<div><h3>Objective</h3><div>Hepatocellular carcinoma (HCC) exhibits a profoundly immunosuppressive microenvironment that limits the efficacy of current immunotherapies. This study evaluated the antitumor activity of unmodified γδ T cells in HCC and defined immune checkpoint–mediated mechanisms that restrict their therapeutic durability.</div></div><div><h3>Methods</h3><div>Bioinformatic analyses of LIHC datasets were performed to identify candidate prognostic T-cell receptor γ variable (TRGV) genes. <em>Ex vivo</em>–expanded γδ T cells were evaluated using <em>in vitro</em> co-culture assays with PD-L1–low (Huh7) and PD-L1–high (HCC-LM3) HCC cell lines, real-time cytotoxicity analyses, and cytokine profiling. Therapeutic efficacy, immune checkpoint regulation, and systemic safety were further assessed in subcutaneous xenograft mouse models using co-implantation and intravenous administration strategies.</div></div><div><h3>Results</h3><div>TRGV3 expression correlated with improved overall survival and reflected γδ T-cell presence within the tumor microenvironment. Unmodified γδ T cells exerted potent, dose-dependent cytotoxicity against HCC cells and suppressed tumor growth <em>in vivo</em>, particularly in PD-L1–negative models. In PD-L1–positive HCC-LM3 tumors, γδ T cell efficacy was reduced following systemic administration and was associated with tumor-induced PD-L1 upregulation, delayed cytotoxicity, and tumor recurrence. Blockade of the PD-L1/PD-1 axis restored durable γδ T cell–mediated tumor control. Importantly, γδ T-cell treatment was well tolerated, with no overt systemic toxicity observed.</div></div><div><h3>Conclusion</h3><div>Unmodified γδ T cells demonstrate strong antitumor activity and a favorable safety profile in HCC but are limited by adaptive PD-L1–mediated immune resistance in PD-L1–positive tumors. These findings provide a mechanistic rationale for combining γδ T cell–based therapies with immune checkpoint inhibition to enhance therapeutic efficacy in advanced HCC.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153163"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124777","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":"Immunological profile of acute Chagas disease patients infected via oral transmission and treated with Benznidazole: a two-year follow-up of immune responses","authors":"Luciane de Freitas Firmino ,&nbsp;Victor Vaitkevicius-Antão ,&nbsp;Amanda Vasconcelos Nascimento ,&nbsp;Cíntia Nascimento Costa-Oliveira ,&nbsp;Michelle da Silva Barros ,&nbsp;Diego José Lira Torres ,&nbsp;Claudeir Dias Silva-Junior ,&nbsp;Byannca de Carvalho Torreão ,&nbsp;Maria Beatriz Araújo Silva ,&nbsp;Carolina de Araújo de Medeiros ,&nbsp;Tayne Fernanda Lemos da Silva ,&nbsp;Maria Aucineide Basílio Albuquerque ,&nbsp;Milena Maria de Morais Silva ,&nbsp;Filipe Prohaska Batista ,&nbsp;Demetrius Montenegro ,&nbsp;Wilson de Oliveira-Júnior ,&nbsp;Cristina Carrazzone ,&nbsp;Silvia Marinho Martins ,&nbsp;Ana Karine Araújo Soares ,&nbsp;Virginia Maria Barros de Lorena","doi":"10.1016/j.imbio.2026.153169","DOIUrl":"10.1016/j.imbio.2026.153169","url":null,"abstract":"<div><div>The state of Pernambuco, Brazil, reported its biggest outbreak of Acute Chagas disease (ACD) caused by oral transmission, in 2019. During the acute phase, timely access to treatment must be quick and performed in all cases, regardless of the transmission route, as approximately 70–80% of cases are cured. Monitoring the immunological profile after Benznidazole (BZ) treatment in ACD patients may help identify tools to support disease progression assessment. This study aimed to evaluate the immune response, especially cytokines and antibodies levels, in patients with ACD and treated with BZ. A total of 28 laboratory-confirmed patients from the outbreak were included. Th1 and Th2 cytokines were quantified in serum samples using flow cytometry, and antibody levels were assessed by indirect immunofluorescence. Our findings indicate that BZ reduced the inflammatory response, as evidenced by decreased levels of Th1-type cytokines (IFN-γ, TNF, IL-2 and IL-6). Anti-inflammatory cytokines (IL-4 and IL-10) also showed a decline following treatment. Only IgM antibody titers were reduced, with no consistent pattern observed for IgG. These results support the use of BZ in acute phase and suggest the potential use of cytokines as auxiliary biomarkers for therapeutic monitoring.</div></div>","PeriodicalId":13270,"journal":{"name":"Immunobiology","volume":"231 2","pages":"Article 153169"},"PeriodicalIF":2.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147305475","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}