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Biomedicines
Special Issues
Autoimmune and Inflammatory Disorders: From Pathogenesis to Therapeutic Targeting
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Autoimmune and Inflammatory Disorders: From Pathogenesis to Therapeutic Targeting

A Special Issue of Biomedicines (ISSN 2227-9059) belonging to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 2334

Editor

Dr. Yu-Wei Chang

E-Mail Website
Guest Editor
Department of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung 402306, Taiwan
Interests: microbiology and immunology; drug repurposing; infodemiology

Special Issue Information

Dear Colleagues,

This Special Issue, “Autoimmune and Inflammatory Disorders: From Pathogenesis to Therapeutic Targeting,” aims to highlight recent advances in understanding immune dysregulation and its therapeutic implications. We welcome original research and reviews focusing on the molecular mechanisms underlying autoimmune and chronic inflammatory diseases, particularly the role of inflammasomes in regulating innate immune responses. Submissions exploring how inflammasome activation contributes to the pathogenesis of sepsis, chronic inflammation, and autoimmune disorders are of particular interest. We also encourage studies proposing strategies to modulate inflammasome activity, such as small-molecule inhibitors, genetic approaches, or upstream signaling modulators, to restore immune balance and ameliorate disease progression. In addition, we invite contributions that investigate the microbiota–immune axis, including how microbial communities, metabolites, or microbe–host interactions regulate immune responses and impact disease development or resolution. Research that links microbiota composition or function with inflammasome regulation or immune tolerance mechanisms will be especially relevant. Overall, this Special Issue seeks to bridge basic mechanistic insights with translational potential, providing a platform for discoveries that advance our understanding of immune-mediated diseases and support the development of novel therapeutic interventions targeting inflammatory and autoimmune pathways.

Dr. Yu-Wei Chang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • inflammasome
  • inflammation
  • sepsis
  • autoimmune
  • microbiota
  • immunomodulation

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Review

22 pages, 5854 KB  
Review
The Role of and Therapeutic Strategies for Eosinophils in Atopic Dermatitis
by Guangyuan Cheng, Suting Sun, Guoshu Deng, Ying Luo, Miao Li, Hang Zhao, Xiaofan Yang, Ruiping Wang, Le Kuai, Ying Zhang, Bin Li, Yi Ru and Jiankun Song
Biomedicines 2026, 14(6), 1212; https://doi.org/10.3390/biomedicines14061212 - 27 May 2026
Viewed by 1134
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease driven by immune dysregulation and epidermal barrier dysfunction, in which eosinophils act as key effector cells contributing to tissue damage and persistent inflammation. This comprehensive review elucidates the multifaceted contributions of eosinophils to the [...] Read more.
Atopic dermatitis (AD) is a chronic inflammatory skin disease driven by immune dysregulation and epidermal barrier dysfunction, in which eosinophils act as key effector cells contributing to tissue damage and persistent inflammation. This comprehensive review elucidates the multifaceted contributions of eosinophils to the progression of AD. Driven by key type 2 cytokines (notably IL-4, IL-5, and IL-13) and specific chemokines, eosinophils infiltrate lesional skin and undergo IgE-mediated degranulation. The subsequent release of cytotoxic granule proteins, including major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil-derived neurotoxin (EDN), and eosinophil peroxidase (EPX), directly induces keratinocyte apoptosis, exacerbates tissue remodeling, and sustains the local inflammatory cascade. Furthermore, we explore the intricate crosstalk between eosinophils and sensory neurons, which, alongside cytokines like IL-31, profoundly aggravates chronic pruritus. Consequently, modulating eosinophil activation and recruitment has emerged as a vital therapeutic approach. We systematically evaluate current and emerging pharmacological interventions, ranging from conventional topical corticosteroids to advanced targeted therapies. Particular emphasis is placed on the mechanistic impact of novel biologics and small-molecule Janus kinase (JAK) inhibitors, demonstrating how they attenuate eosinophilic inflammation. By identifying current gaps in this field, this review provides valuable insights for future research and clinical practice in the field of AD. Full article
(This article belongs to the Special Issue Autoimmune and Inflammatory Disorders: From Pathogenesis to Therapeutic Targeting)
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Graphical abstract

25 pages, 3467 KB  
Review
Glaucoma and Autoimmunity: Immunopathogenic Mechanisms and Emerging Immunomodulatory Therapies
by Murong Wang, Chunying Liu and Xin Wei
Biomedicines 2026, 14(6), 1209; https://doi.org/10.3390/biomedicines14061209 - 27 May 2026
Viewed by 794
Abstract
Glaucoma is a chronic progressive optic neuropathy and one of the leading causes of irreversible blindness worldwide. Although elevated intraocular pressure remains the most important modifiable risk factor, increasing evidence suggests that immune dysregulation and autoimmune responses also contribute substantially to disease onset [...] Read more.
Glaucoma is a chronic progressive optic neuropathy and one of the leading causes of irreversible blindness worldwide. Although elevated intraocular pressure remains the most important modifiable risk factor, increasing evidence suggests that immune dysregulation and autoimmune responses also contribute substantially to disease onset and progression. Clinical studies across different glaucoma subtypes have identified subtype-dependent immune abnormalities, including altered serum autoantibody profiles, dysregulated cytokine and chemokine expression, and changes in peripheral immune cell subsets. Experimental and translational studies further indicate that multiple immunopathogenic mechanisms are involved in glaucomatous neurodegeneration, including glial cell-mediated immune responses, activation of pattern recognition receptor signalling pathways, adaptive immune responses, and complement cascade dysregulation. These processes may interact to sustain chronic neuroinflammation, promote retinal ganglion cell injury, and accelerate optic nerve degeneration. Importantly, a better understanding of immune involvement in glaucoma has generated growing interest in immunomodulatory therapy as a potential strategy beyond intraocular pressure lowering. Targeting microglial activation, inflammatory signalling pathways, adaptive immune imbalance, and complement-mediated injury has shown neuroprotective potential in animal or in vitro models, whereas clinical evidence in glaucoma patients remains limited. These findings may provide preliminary directions for future therapeutic development. In this review, we summarise the current clinical evidence linking glaucoma with autoimmunity, discuss the major immune mechanisms implicated in disease pathogenesis, and highlight recent advances in immunomodulatory therapeutic strategies. Elucidating the immune basis of glaucoma may help pave the way for more precise and effective treatments for this complex optic neuropathy. We believe that immune dysregulation in glaucoma functions as a context-dependent amplifier of retinal ganglion cell injury rather than a uniform primary driver, with innate (microglia/astrocytes), adaptive (T/B cells, HSP-specific immunity), and complement pathways interacting to sustain neuroinflammation and neurodegeneration. This integrated immune response contributes to subtype- and stage-specific vulnerability, and targeting these maladaptive immune mechanisms represents a promising, precision-guided strategy for neuroprotection beyond intraocular pressure lowering. Full article
(This article belongs to the Special Issue Autoimmune and Inflammatory Disorders: From Pathogenesis to Therapeutic Targeting)
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