Pub Date : 2025-11-24DOI: 10.1016/j.imlet.2025.107115
Waldemar Rastawicki , Aleksandra Anna Zasada
Vaccination plays a key role in the prevention of pertussis, the infectious disease that is endemic worldwide. Two types of pertussis vaccines are currently in use: whole-cell (wP) and acellular (aP) vaccines. Differences in the duration of immunity have been observed depending on the vaccine type. In this study, the levels of individual IgG subclasses and antibody avidity were assessed in children vaccinated with either aP or wP vaccines. The results revealed no significant differences in the mean IgG antibody levels and avidity between children immunised with wP and those who received aP vaccines. However, in the vaccinated children IgG4 was a dominated IgG subclass, regardless of vaccine used (aP v. wP), whereas in pertussis patients the IgG1 was dominating. These findings need deeper investigation, in terms of a vaccine efficacy and wanning immunity, as typically in response to protein antigens IgG1 is dominating. Moreover, the observation of IgG4 predominance in vaccinated vs. IgG1 predominance in infected individuals might be a valuable parameter in pertussis diagnostics as it enables differentiation between infected and vaccinated but not-infected individuals.
{"title":"Comparison of IgG antibody levels, avidity, and subclass distribution against pertussis toxin in children and adolescents after four-dose primary whole-cell (DTwP) or acellular (DTaP) vaccination, each followed by a single DTaP booster","authors":"Waldemar Rastawicki , Aleksandra Anna Zasada","doi":"10.1016/j.imlet.2025.107115","DOIUrl":"10.1016/j.imlet.2025.107115","url":null,"abstract":"<div><div>Vaccination plays a key role in the prevention of pertussis, the infectious disease that is endemic worldwide. Two types of pertussis vaccines are currently in use: whole-cell (wP) and acellular (aP) vaccines. Differences in the duration of immunity have been observed depending on the vaccine type. In this study, the levels of individual IgG subclasses and antibody avidity were assessed in children vaccinated with either aP or wP vaccines. The results revealed no significant differences in the mean IgG antibody levels and avidity between children immunised with wP and those who received aP vaccines. However, in the vaccinated children IgG4 was a dominated IgG subclass, regardless of vaccine used (aP v. wP), whereas in pertussis patients the IgG1 was dominating. These findings need deeper investigation, in terms of a vaccine efficacy and wanning immunity, as typically in response to protein antigens IgG1 is dominating. Moreover, the observation of IgG4 predominance in vaccinated vs. IgG1 predominance in infected individuals might be a valuable parameter in pertussis diagnostics as it enables differentiation between infected and vaccinated but not-infected individuals.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107115"},"PeriodicalIF":2.8,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145623053","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}
Pub Date : 2025-11-23DOI: 10.1016/j.imlet.2025.107112
Saaz Kumar , Yashpal Jesswani , Manaish Kumar
{"title":"Letter to the editor: \"Importance of BCG vaccination at birth in pediatric patients with chronic granulomatous disease after hematopoietic stem cell transplantation in developing countries\"","authors":"Saaz Kumar , Yashpal Jesswani , Manaish Kumar","doi":"10.1016/j.imlet.2025.107112","DOIUrl":"10.1016/j.imlet.2025.107112","url":null,"abstract":"","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107112"},"PeriodicalIF":2.8,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145603906","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}
Dendritic cells (DCs) are highly efficient antigen-presenting cells that play a central role in inducing and controlling immune responses. Beyond their role in antigen presentation and in orchestrating lymphocyte activities, DCs also contribute to the spatial and functional organization of lymphoid structures, including both secondary and tertiary lymphoid organs, acting at different levels during both lymphoid tissue neogenesis and their maintenance.
DCs can facilitate lymphoid tissue development by interacting with both lymphoid tissue inducer and organizer cells, initiating early aggregation and supporting lymphotoxin-mediated signaling pathways essential for lymphoid structure maturation. Additionally, DCs release chemokines attracting and anchoring immune cells in lymphoid tissues and regulate the formation and the overall size of high endothelial venule system, which mediate immune cell trafficking into lymphoid tissues.
The dynamic crosstalk between DCs and fibroblastic reticular cells (FRC), which facilitate immune cell interactions and compartmentalization, is essential for lymphoid tissue specialization and function, though the precise cellular and molecular mechanisms of DC/FRC crosstalk remain to be fully elucidated.
Finally, studies in mice and humans suggest that DC subsets are pivotal in T follicular helper cell differentiation, essential for humoral immunity in B cell follicles of lymphoid tissues, therefore emphasizing DCs’ critical role also in supporting B cell maturation and antibody responses in the germinal centers of lymphoid organs.
{"title":"Dendritic Cells: key controllers of lymphoid tissue organization","authors":"Alessia Calabrò , Claudia De Pasquale , Fabiana Drommi , Elena Giusto , Silvia Tamburini , Grazia Vento , Sayuri Yamazaki , Stefania Campana , Guido Ferlazzo","doi":"10.1016/j.imlet.2025.107111","DOIUrl":"10.1016/j.imlet.2025.107111","url":null,"abstract":"<div><div>Dendritic cells (DCs) are highly efficient antigen-presenting cells that play a central role in inducing and controlling immune responses. Beyond their role in antigen presentation and in orchestrating lymphocyte activities, DCs also contribute to the spatial and functional organization of lymphoid structures, including both secondary and tertiary lymphoid organs, acting at different levels during both lymphoid tissue neogenesis and their maintenance.</div><div>DCs can facilitate lymphoid tissue development by interacting with both lymphoid tissue inducer and organizer cells, initiating early aggregation and supporting lymphotoxin-mediated signaling pathways essential for lymphoid structure maturation. Additionally, DCs release chemokines attracting and anchoring immune cells in lymphoid tissues and regulate the formation and the overall size of high endothelial venule system, which mediate immune cell trafficking into lymphoid tissues.</div><div>The dynamic crosstalk between DCs and fibroblastic reticular cells (FRC), which facilitate immune cell interactions and compartmentalization, is essential for lymphoid tissue specialization and function, though the precise cellular and molecular mechanisms of DC/FRC crosstalk remain to be fully elucidated.</div><div>Finally, studies in mice and humans suggest that DC subsets are pivotal in T follicular helper cell differentiation, essential for humoral immunity in B cell follicles of lymphoid tissues, therefore emphasizing DCs’ critical role also in supporting B cell maturation and antibody responses in the germinal centers of lymphoid organs.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107111"},"PeriodicalIF":2.8,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530634","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":"Addressing the immunological gaps in asthma treatment: A call for region-specific research in Africa","authors":"Zemichael Getu Alemayehu, Brook Lelisa Sime, Abenezer Shiferaw Keraga","doi":"10.1016/j.imlet.2025.107110","DOIUrl":"10.1016/j.imlet.2025.107110","url":null,"abstract":"","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107110"},"PeriodicalIF":2.8,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145512572","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}
Pub Date : 2025-11-07DOI: 10.1016/j.imlet.2025.107109
Ajith Cherian , Divya K P , Amod R , Deepa K P
Background
Movement disorders, as an anti-neuronal antibody mediated neurological syndrome(ANNS), is usually associated with anti-CV2/CRMP5,Hu/ANNA1 and Contactin-associated protein-like 2 (CASPR2) antibodies. Anti-Yo antibody associated movement disorders are extremely rare.
Methods
We analysed the data of 47 patients with anti –Yo antibodies who presented over a period of 5 years (2019–2024) in a tertiary care institute. Those with movement disorder phenotype, without ataxia, were included. Other etiologies were excluded with relevant work up.
Results
We report two elderly males in their sixties who presented with a subacute onset isolated progressive axial movement disorders, with positive anti-Yo antibody. One patient with axial myoclonus and camptocormia who did not initially respond to intravenous methylprednisolone had remarkable improvement with intravenous immunoglobulin and rituximab, while in the other treatment response was suboptimal.
Conclusion
Movement disorders due to anti-neuronal antibodies should be suspected when they develop subacutely, in older patients (> 50 years), have a progressive course beyond 3 months, associated with pain and constitutional symptoms like weight loss, all of which were present in our cases. Such intracellular Yo antigen induced ANNS usually have guarded response to immunomodulatory therapy compared to those mediated by antibodies against surface antigens, though one patient of ours had a remarkable improvement.
{"title":"Anti-Yo antibody associated axial movement disorders – a novel phenotype in ANNS","authors":"Ajith Cherian , Divya K P , Amod R , Deepa K P","doi":"10.1016/j.imlet.2025.107109","DOIUrl":"10.1016/j.imlet.2025.107109","url":null,"abstract":"<div><h3>Background</h3><div>Movement disorders, as an anti-neuronal antibody mediated neurological syndrome(ANNS), is usually associated with anti-CV2/CRMP5,Hu/ANNA1 and Contactin-associated protein-like 2 (CASPR2) antibodies. Anti-Yo antibody associated movement disorders are extremely rare.</div></div><div><h3>Methods</h3><div>We analysed the data of 47 patients with anti –Yo antibodies who presented over a period of 5 years (2019–2024) in a tertiary care institute. Those with movement disorder phenotype, without ataxia, were included. Other etiologies were excluded with relevant work up.</div></div><div><h3>Results</h3><div>We report two elderly males in their sixties who presented with a subacute onset isolated progressive axial movement disorders, with positive anti-Yo antibody. One patient with axial myoclonus and camptocormia who did not initially respond to intravenous methylprednisolone had remarkable improvement with intravenous immunoglobulin and rituximab, while in the other treatment response was suboptimal.</div></div><div><h3>Conclusion</h3><div>Movement disorders due to anti-neuronal antibodies should be suspected when they develop subacutely, in older patients (> 50 years), have a progressive course beyond 3 months, associated with pain and constitutional symptoms like weight loss, all of which were present in our cases. Such intracellular Yo antigen induced ANNS usually have guarded response to immunomodulatory therapy compared to those mediated by antibodies against surface antigens, though one patient of ours had a remarkable improvement.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107109"},"PeriodicalIF":2.8,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145481997","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}
Pub Date : 2025-11-06DOI: 10.1016/j.imlet.2025.107108
François-Xavier Mauvais , Peter van Endert
Macrophages expressing the sialic acid-binding lectin Siglec-1 are positioned strategically for uptake and filtering of antigenic material circulating through the lymphatic system into the subcapsular sinus of lymph nodes and through the blood into the marginal zone of the spleen. Siglec-1+ macrophages are also found in many tissues, frequently displaying an inflammatory profile. In secondary lymphoid organs, these cells are strategically positioned and play a role in adaptive immune responses by B, NK and T lymphocytes. A potential role of the cells in antitumor immunity has attracted significant scientific interest. This concept is supported by a report of dendritic cell-independent priming of a protective antitumor response by lymph node Siglec-1+ macrophages. Indeed, examination of preclinical models and human tumors has provided evidence for a dominant protective effect of lymph node Siglec-1+ macrophages in major types of solid tumors e.g. breast or colorectal cancer. In contrast, Siglec-1+ macrophages within tumor tissue have been found to be associated variably with favorable or unfavorable outcome depending on the model and tumor studied. We have recently demonstrated in mouse models that splenic Siglec-1+ macrophages in themarginal zone can prime protective tumor immunity against both tumors disseminating through the blood and tumors invading the spleen in the absence of type 1 conventional dendritic cells. Considering this, we postulate Siglec-1+ macrophages in all secondary lymphoid organs can prime potent antitumor responses. We propose that this capacity could be exploited for therapeutic stimulation of tumor immunity.
{"title":"Siglec-1+ macrophages in anti-tumor immunity","authors":"François-Xavier Mauvais , Peter van Endert","doi":"10.1016/j.imlet.2025.107108","DOIUrl":"10.1016/j.imlet.2025.107108","url":null,"abstract":"<div><div>Macrophages expressing the sialic acid-binding lectin Siglec-1 are positioned strategically for uptake and filtering of antigenic material circulating through the lymphatic system into the subcapsular sinus of lymph nodes and through the blood into the marginal zone of the spleen. Siglec-1<sup>+</sup> macrophages are also found in many tissues, frequently displaying an inflammatory profile. In secondary lymphoid organs, these cells are strategically positioned and play a role in adaptive immune responses by B, NK and T lymphocytes. A potential role of the cells in antitumor immunity has attracted significant scientific interest. This concept is supported by a report of dendritic cell-independent priming of a protective antitumor response by lymph node Siglec-1+ macrophages. Indeed, examination of preclinical models and human tumors has provided evidence for a dominant protective effect of lymph node Siglec-1+ macrophages in major types of solid tumors e.g. breast or colorectal cancer. In contrast, Siglec-1+ macrophages within tumor tissue have been found to be associated variably with favorable or unfavorable outcome depending on the model and tumor studied. We have recently demonstrated in mouse models that splenic Siglec-1+ macrophages in themarginal zone can prime protective tumor immunity against both tumors disseminating through the blood and tumors invading the spleen in the absence of type 1 conventional dendritic cells. Considering this, we postulate Siglec-1+ macrophages in all secondary lymphoid organs can prime potent antitumor responses. We propose that this capacity could be exploited for therapeutic stimulation of tumor immunity.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107108"},"PeriodicalIF":2.8,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145476772","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}
To investigate the pro-inflammatory role and underlying mechanism of Perilipin 2 (PLIN2) in Allergic Rhinitis (AR), focusing on its regulation of PINK1/Parkin-mediated mitophagy and the subsequent impact on lipid metabolism and oxidative stress.
Methods
Single-cell RNA sequencing (scRNA-seq) analysis was performed using GSE261706 from the GEO database, involving nasal mucosa from AR patients and healthy controls. A murine AR model was induced by ovalbumin (OVA), and human nasal epithelial cells (HNEpCs) were stimulated with Der p1. Interventions included AAV-mediated PLIN2 knockdown in vivo and siRNA-mediated knockdown in vitro. Techniques included Western blotting, qRT-PCR, flow cytometry, ELISA, and immunofluorescence/histological staining to assess PLIN2 expression, mitophagy, lipid accumulation, oxidative stress, and inflammatory responses.
Results
scRNA-seq analysis identified PLIN2 as a significantly upregulated gene in AR epithelial cells, which correlated with dysfunctional autophagy pathways. In both OVA-induced mice and Der p1-treated HNEpCs, PLIN2 expression was significantly elevated, accompanied by inhibited mitophagy (decreased LC3-II/I ratio, reduced PINK1/Parkin levels, and p62 accumulation), increased lipid deposition, and elevated ROS levels. PLIN2 knockdown markedly ameliorated AR pathology in mice, reducing inflammatory infiltration and serum levels of IgE, IL-4, and IL-5. Mechanistically, PLIN2 knockdown restored PINK1/Parkin-mediated mitophagy, decreased lipid accumulation, and attenuated ROS-induced cellular damage in HNEpCs.
Conclusions
PLIN2 exacerbates AR pathogenesis by inhibiting PINK1/Parkin-mediated mitophagy, promoting lipid accumulation and oxidative stress, and ultimately causing cellular damage in nasal epithelial cells. PLIN2 acts as a pivotal mediator linking metabolic dysregulation to inflammation, highlighting it as a promising therapeutic target for AR treatment.
{"title":"PLIN2 exacerbates Allergic Rhinitis by inhibiting PINK1/Parkin-mediated mitophagy","authors":"Wangbo Yu , Shuai Zhang , Lijuan Peng , Jingwei Du","doi":"10.1016/j.imlet.2025.107107","DOIUrl":"10.1016/j.imlet.2025.107107","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the pro-inflammatory role and underlying mechanism of Perilipin 2 (PLIN2) in Allergic Rhinitis (AR), focusing on its regulation of PINK1/Parkin-mediated mitophagy and the subsequent impact on lipid metabolism and oxidative stress.</div></div><div><h3>Methods</h3><div>Single-cell RNA sequencing (scRNA-seq) analysis was performed using GSE261706 from the GEO database, involving nasal mucosa from AR patients and healthy controls. A murine AR model was induced by ovalbumin (OVA), and human nasal epithelial cells (HNEpCs) were stimulated with Der p1. Interventions included AAV-mediated PLIN2 knockdown in vivo and siRNA-mediated knockdown in vitro. Techniques included Western blotting, qRT-PCR, flow cytometry, ELISA, and immunofluorescence/histological staining to assess PLIN2 expression, mitophagy, lipid accumulation, oxidative stress, and inflammatory responses.</div></div><div><h3>Results</h3><div>scRNA-seq analysis identified PLIN2 as a significantly upregulated gene in AR epithelial cells, which correlated with dysfunctional autophagy pathways. In both OVA-induced mice and Der p1-treated HNEpCs, PLIN2 expression was significantly elevated, accompanied by inhibited mitophagy (decreased LC3-II/I ratio, reduced PINK1/Parkin levels, and p62 accumulation), increased lipid deposition, and elevated ROS levels. PLIN2 knockdown markedly ameliorated AR pathology in mice, reducing inflammatory infiltration and serum levels of IgE, IL-4, and IL-5. Mechanistically, PLIN2 knockdown restored PINK1/Parkin-mediated mitophagy, decreased lipid accumulation, and attenuated ROS-induced cellular damage in HNEpCs.</div></div><div><h3>Conclusions</h3><div>PLIN2 exacerbates AR pathogenesis by inhibiting PINK1/Parkin-mediated mitophagy, promoting lipid accumulation and oxidative stress, and ultimately causing cellular damage in nasal epithelial cells. PLIN2 acts as a pivotal mediator linking metabolic dysregulation to inflammation, highlighting it as a promising therapeutic target for AR treatment.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"278 ","pages":"Article 107107"},"PeriodicalIF":2.8,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145451700","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}
Pub Date : 2025-11-03DOI: 10.1016/j.imlet.2025.107106
Franziska Maria Schmidt , Marta Rizzi
The B cell compartment is maintained by continuous replenishment from hematopoietic stem cells (HSCs) and multipotent progenitors, as well as from B cell precursors. B cell depletion is a common therapeutic approach, not only in the context of B cell malignancies, but also in autoimmunity. The targeted elimination of B cells can be achieved through the use of chimeric antigen receptor (CAR)-T cells or monoclonal antibodies or bispecific antibodies that target both B and NK cells or B and T cells. When B cells are depleted, repopulation from bone marrow precursors occurs within three months to one year, following ontogeny. Nevertheless, prolonged B cell aplasia is observed in some patients and is associated with a progressive reduction of serum immunoglobulins and an increased susceptibility to infections. The mechanisms underlying such defects in B cell replenishment remain to be fully elucidated and studies on human B lymphopoiesis are needed in this context. Mouse models can be helpful in studying mechanisms of B cell development and the role of multiple (B cell-specific) genes in this process; however, they do not always mirror the human developmental dynamics and signals. Hence further tools are needed to study human B lymphopoiesis defects. In this review, we summarize the reported studies and cases of prolonged B cell aplasia following B cell depletion and discuss potential underlying causes. We then provide a comprehensive overview of the various in vitro models that can be used to study the dynamic of B lymphopoiesis to dissect B cell developmental defects in humans.
{"title":"Human B-lymphopoiesis: Clinical challenges in B cell reconstitution and advances in in vitro modeling","authors":"Franziska Maria Schmidt , Marta Rizzi","doi":"10.1016/j.imlet.2025.107106","DOIUrl":"10.1016/j.imlet.2025.107106","url":null,"abstract":"<div><div>The B cell compartment is maintained by continuous replenishment from hematopoietic stem cells (HSCs) and multipotent progenitors, as well as from B cell precursors. B cell depletion is a common therapeutic approach, not only in the context of B cell malignancies, but also in autoimmunity. The targeted elimination of B cells can be achieved through the use of chimeric antigen receptor (CAR)-T cells or monoclonal antibodies or bispecific antibodies that target both B and NK cells or B and T cells. When B cells are depleted, repopulation from bone marrow precursors occurs within three months to one year, following ontogeny. Nevertheless, prolonged B cell aplasia is observed in some patients and is associated with a progressive reduction of serum immunoglobulins and an increased susceptibility to infections. The mechanisms underlying such defects in B cell replenishment remain to be fully elucidated and studies on human B lymphopoiesis are needed in this context. Mouse models can be helpful in studying mechanisms of B cell development and the role of multiple (B cell-specific) genes in this process; however, they do not always mirror the human developmental dynamics and signals. Hence further tools are needed to study human B lymphopoiesis defects. In this review, we summarize the reported studies and cases of prolonged B cell aplasia following B cell depletion and discuss potential underlying causes. We then provide a comprehensive overview of the various <em>in vitro</em> models that can be used to study the dynamic of B lymphopoiesis to dissect B cell developmental defects in humans.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107106"},"PeriodicalIF":2.8,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145451722","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}
Pub Date : 2025-10-25DOI: 10.1016/j.imlet.2025.107105
Nan Wang , Xingyue Zheng , Qianzi Ma , Yanlu Che , Wanchao Yang , Zhen Liu , Jingting Wang
<div><h3>Background</h3><div>Hydrogen is known to improve allergic rhinitis. Nasal microbiota that are different from those of healthy normal subjects have been detected in the nasal cavity of patients with allergic rhinitis (AR), and the microbiota can influence the metabolic levels of both themselves and their hosts. In addition, hydrogen has been shown to affect microbiota distribution and diversity. These findings suggest that hydrogen may target the nasal microbiota and metabolites to treat AR. Therefore, further in-depth exploration of the specific mechanism of action of hydrogen in the treatment of allergic rhinitis is necessary to provide a more scientific and effective program for the treatment of this disease. In this study, 35 patients with allergic rhinitis were selected as the experimental group, namely the HI group, and 35 healthy individuals were selected as the control group, namely the HC group.</div></div><div><h3>Methods</h3><div>The serum eosinophil count (EOS), immunoglobulin E (IgE) concentration, visual analogue scale (VAS) score, total nasal symptom score (TNSS), and rhinoconjunctivitis quality of life questionnaire (RQLQ) were used before and after hydrogen inhalation in AR patients. The skin prick test (SPT) was used to determine allergen sensitization. The community composition and relative abundance of the nasal microbiota were examined before and after hydrogen inhalation and in healthy subjects via 16S rRNA gene sequencing. Liquid chromatography‒mass spectrometry (LC‒MS) was used to explore the metabolic profile.</div></div><div><h3>Results</h3><div>There were no adverse reactions during or after hydrogen inhalation in AR patients, and the safety was good, with significant improvements in the VAS, TNSS, EOS, and IgE scores (<em>P</em> < 0.05). The results of 16S rRNA gene sequencing of nasal microbiota revealed that the distribution and diversity of nasal microbiota in AR patients were significantly altered after hydrogen inhalation compared with those before hydrogen inhalation and were closer to those of normal individuals. We also found that the metabolites 19(<em>R</em>)‑hydroxy-prostaglandin E2, arachidonic acid (AA), LEP 20:2, LEP O-18:2, LEP O-22:3, LPS 18:1, and LPS 20:3 were significantly more abundant than normal in nasal secretions in AR and then significantly decreased and approached normal levels after being modulated by hydrogen. 19(<em>R</em>)-Hydroxy-prostaglandin E2 levels were positively correlated with the abundance of Devosia, Paenibacillus, and colonies in the nasal cavity. AA was significantly positively correlated with Muribaculum bacteria and negatively correlated with [Eubacterium]_ruminantium_group. LPE was positively correlated with the bacteria Paenibacillus and Muribaculum and negatively correlated with [Eubacterium]_ruminantium_group. LPS was negatively correlated with [Eubacterium]_ruminantium_group and UCG-002 and positively correlated with Devosia and Muribaculum.</div></div><div><
{"title":"Hydrogen therapy modulates nasal microbiota and metabolites in allergic rhinitis patients","authors":"Nan Wang , Xingyue Zheng , Qianzi Ma , Yanlu Che , Wanchao Yang , Zhen Liu , Jingting Wang","doi":"10.1016/j.imlet.2025.107105","DOIUrl":"10.1016/j.imlet.2025.107105","url":null,"abstract":"<div><h3>Background</h3><div>Hydrogen is known to improve allergic rhinitis. Nasal microbiota that are different from those of healthy normal subjects have been detected in the nasal cavity of patients with allergic rhinitis (AR), and the microbiota can influence the metabolic levels of both themselves and their hosts. In addition, hydrogen has been shown to affect microbiota distribution and diversity. These findings suggest that hydrogen may target the nasal microbiota and metabolites to treat AR. Therefore, further in-depth exploration of the specific mechanism of action of hydrogen in the treatment of allergic rhinitis is necessary to provide a more scientific and effective program for the treatment of this disease. In this study, 35 patients with allergic rhinitis were selected as the experimental group, namely the HI group, and 35 healthy individuals were selected as the control group, namely the HC group.</div></div><div><h3>Methods</h3><div>The serum eosinophil count (EOS), immunoglobulin E (IgE) concentration, visual analogue scale (VAS) score, total nasal symptom score (TNSS), and rhinoconjunctivitis quality of life questionnaire (RQLQ) were used before and after hydrogen inhalation in AR patients. The skin prick test (SPT) was used to determine allergen sensitization. The community composition and relative abundance of the nasal microbiota were examined before and after hydrogen inhalation and in healthy subjects via 16S rRNA gene sequencing. Liquid chromatography‒mass spectrometry (LC‒MS) was used to explore the metabolic profile.</div></div><div><h3>Results</h3><div>There were no adverse reactions during or after hydrogen inhalation in AR patients, and the safety was good, with significant improvements in the VAS, TNSS, EOS, and IgE scores (<em>P</em> < 0.05). The results of 16S rRNA gene sequencing of nasal microbiota revealed that the distribution and diversity of nasal microbiota in AR patients were significantly altered after hydrogen inhalation compared with those before hydrogen inhalation and were closer to those of normal individuals. We also found that the metabolites 19(<em>R</em>)‑hydroxy-prostaglandin E2, arachidonic acid (AA), LEP 20:2, LEP O-18:2, LEP O-22:3, LPS 18:1, and LPS 20:3 were significantly more abundant than normal in nasal secretions in AR and then significantly decreased and approached normal levels after being modulated by hydrogen. 19(<em>R</em>)-Hydroxy-prostaglandin E2 levels were positively correlated with the abundance of Devosia, Paenibacillus, and colonies in the nasal cavity. AA was significantly positively correlated with Muribaculum bacteria and negatively correlated with [Eubacterium]_ruminantium_group. LPE was positively correlated with the bacteria Paenibacillus and Muribaculum and negatively correlated with [Eubacterium]_ruminantium_group. LPS was negatively correlated with [Eubacterium]_ruminantium_group and UCG-002 and positively correlated with Devosia and Muribaculum.</div></div><div><","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107105"},"PeriodicalIF":2.8,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145415791","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}
Pub Date : 2025-10-12DOI: 10.1016/j.imlet.2025.107104
Apostolos Taxiarchis , Jovan Antovic , Olav Rooyackers , Gabriel Dumitrescu
This case report analyzes two severe COVID-19 patients without pulmonary embolism, revealing persistently elevated levels of extracellular vesicles (EVs) carrying tissue factor (TF+), complement proteins (C3a+, TCC+), and endothelial markers (CD144+, CD54+). Temporal trends in these EV subpopulations correlated with clinical deterioration, suggesting their role in endothelial injury, complement hyperactivation, and thromboinflammation. Notably, TF+EV dynamics aligned with anticoagulant treatment responses, while MPO+EVs reflected neutrophil activity without thrombotic complications. Despite differences in patient characteristics, these findings propose that patient-specific EV profiles may serve as potential indicators of disease progression, warranting targeted studies to validate their biomarker potential in severe COVID-19.
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