New Insights in Immunological Pathways

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 1404

Special Issue Editor


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Guest Editor
1. Department of Clinical Pathology, Medical Research, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation No. 289, Jianguo Road, Xindian District, New Taipei City 231, Taiwan
2. Department of Biotechnology, Ming Chuan University, Taoyuan City 333, Taiwan
Interests: immunology; oncology; vaccinology

Special Issue Information

Dear Colleagues,

The field of immunology has witnessed remarkable advancements in recent years, shedding light on the intricate mechanisms that govern our immune system's response to various stimuli. The Special Issue "New Insights in Immunological Pathways" aims to bring together cutting-edge research that explores these pathways, offering novel perspectives and groundbreaking discoveries.

This Special Issue welcomes contributions that delve into the latest findings in immunological research, including but not limited to, the role of immune cells in tissue repair and regeneration, the interplay between innate and adaptive immunity, the immune pathways against different types of pathogens, and the mechanisms underlying autoimmune diseases. Researchers are encouraged to submit research articles, and review articles that present novel insights, challenge existing paradigms, or provide comprehensive overviews of emerging fields. One of the key objectives of this issue is to foster interdisciplinary collaborations among researchers from diverse backgrounds, thereby accelerating the pace of scientific discovery. By grouping papers by topic, we aim to facilitate efficient navigation through the broad scope of immunological research, making it easier for scholars to identify and engage with relevant work.

We invite you to contribute to this exciting endeavor and join us in advancing the frontiers of immunological knowledge.

Dr. Wan-Chung Hu
Guest Editor

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Keywords

  • immune response
  • immune signal pathway
  • cytokine storm

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Published Papers (1 paper)

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Research

21 pages, 4298 KB  
Article
Upregulated ZBP1 Is Associated with B-Cell Dysregulation in Systemic Lupus Erythematosus
by Yiying Yang, Ke Liu, Hao Ma, Litao Lu, Ganqian Zhu, Xiaoxia Zuo, Huali Zhang, Yaxi Zhu and Muyao Guo
Biomedicines 2026, 14(2), 451; https://doi.org/10.3390/biomedicines14020451 - 17 Feb 2026
Viewed by 1092
Abstract
Background/Objectives: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by B-cell hyperactivation and excessive autoantibody production. Z-DNA binding protein 1 (ZBP1), an innate immune sensor involved in nucleic acid recognition and cell death signaling, has been implicated in antiviral and inflammatory responses. [...] Read more.
Background/Objectives: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by B-cell hyperactivation and excessive autoantibody production. Z-DNA binding protein 1 (ZBP1), an innate immune sensor involved in nucleic acid recognition and cell death signaling, has been implicated in antiviral and inflammatory responses. However, its role in B-cell dysregulation during SLE remains unclear. Methods: Integrative transcriptomic analyses were performed using public datasets (GSE61635, GSE235658, GSE136035, and GSE163497) to determine the expression pattern and biological functions of ZBP1 in SLE. Bulk RNA-seq and single-cell RNA-seq data were used to evaluate ZBP1 expression across B-cell subsets. Correlations between ZBP1 expression, disease activity, and immunological parameters were assessed. RNA-seq data following ZBP1 knockdown were analyzed to explore its potential downstream pathways and molecular networks. In addition, in vitro ZBP1 knockdown experiments were conducted to examine its effects on B-cell activation, plasma cell differentiation, and antibody production. Results: ZBP1 was significantly upregulated in peripheral blood and B cells from SLE patients and was enriched in pathways related to type I interferon signaling and cytokine-mediated immune responses. Single-cell transcriptomic profiling further revealed elevated ZBP1 expression across multiple B-cell subsets, including naïve B cells, memory B cells, age-associated B cells (ABCs), and plasma cells. Clinically, ZBP1 expression in peripheral B cells was positively correlated with CD86 mean fluorescence intensity (MFI), SLE Disease Activity Index (SLEDAI) scores, and serum IgG levels, suggesting a link between ZBP1 and B-cell activation. RNA-seq analysis following ZBP1 silencing demonstrated that ZBP1 regulates genes involved in the cell cycle, DNA replication, and p53 signaling, indicating its potential role in promoting B-cell proliferation and activation. Functionally, ZBP1 silencing impaired B-cell activation, reduced plasma cell differentiation, and decreased immunoglobulin production in vitro. Conclusions: Our study identifies ZBP1 as a molecule upregulated in SLE B cells and associated with B-cell activation and disease activity. Although direct causality remains to be established, the data indicate that ZBP1 may contribute to SLE pathogenesis by modulating cell cycle-related pathways and promoting aberrant B-cell responses, highlighting its potential as a biomarker and a candidate therapeutic target in SLE. Full article
(This article belongs to the Special Issue New Insights in Immunological Pathways)
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