Innate Immunomodulation and Inflammation: From Molecular Mechanisms to Pre-Clinical Insights

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 4868

Special Issue Editors


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Guest Editor
Centre for Immunobiology and Regenerative Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AD, UK
Interests: mast cell biology; inflammation; innate immunity at the oral mucosa

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Guest Editor
Department of Medicine, Center of Excellence for Inflammation, Infectious Diseases, and Immunity, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA
Interests: the interaction between chronic viral infections and the host innate immune system in carcinogenesis; type I interferons-mediated innate immune system; DNA damage response; autophagy; oxidative stress
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Guest Editor
Department of Laboratory Medicine and Hospital Hygiene, Robert-Bosch-Hospital, Auerbachstr. 110, 70736 Stuttgart, Germany
Interests: atherosclerosis; aortic valve sclerosis; innate immunity; modified lipoproteins

Special Issue Information

Dear Colleagues,

We are pleased to invite you to submit and contribute with your original research and review articles to the upcoming Special Issue, “Innate Immunomodulation and Inflammation,” in the peer-reviewed, open access journal Biomolecules.

The innate immune system constitutes the first line of defense that offers immediate protection against bacterial and viral infection. Further, cells of the innate immune system recognize “danger” signals generated following cell stress, injury and trauma, aging, and cancer. Once activated, innate immunity plays a fundamental role in priming the adaptive immune system for specific and targeted responses that contribute to tissue repair, good health, and survival.

In recent years, there has been an increased understanding of mediators of inflammatory responses and the role of immune checkpoints in the modulation of immune responses. This has led to the development of effective biological agents and therapies that enhance the function of T cells. However, it has now become evident that modulating the function of innate immune cells can also have therapeutic effects. Exciting new studies are providing evidence to support the notion that targeting co-inhibitory or co-stimulatory receptors on innate immune cells, or even modulation of the microbiome, has remarkable potential for therapies not only in cancer but also in autoimmune disease, inflammation, and chronic infection.

The aims of this Special Issue are as follows:

  • To define new biomarkers for diseases associated with innate immune cells.
  • To highlight novel studies on the characterization of the pharmacological mechanisms of new drugs targeting innate immune cells.
  • To showcase the potential of new approaches to modulate innate immune responses for the development of therapies for cancer, autoimmunity, inflammation, and chronic infectious diseases.

For this Special Issue, basic research, in vitro and in vivo investigations, and pre-clinical studies examining the effects of innate cell modulation are welcome.

We look forward to receiving your contributions.

Dr. Fabián Flores-Borja
Dr. Shunbin Ning
Prof. Dr. Michael Torzewski
Guest Editors

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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules 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 2700 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

  • innate immunity
  • therapy
  • immune checkpoints
  • cancer
  • autoimmunity
  • inflammation
  • infection
  • danger-associated molecular patterns
  • pattern recognition receptors

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Published Papers (3 papers)

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Research

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33 pages, 4788 KiB  
Article
Effects of Pressure, Hypoxia, and Hyperoxia on Neutrophil Granulocytes
by Richard F. Kraus, Daniel Panter, Michael A. Gruber, Stephanie Arndt, Petra Unger, Michael T. Pawlik and Diane Bitzinger
Biomolecules 2024, 14(10), 1242; https://doi.org/10.3390/biom14101242 - 30 Sep 2024
Cited by 1 | Viewed by 1863
Abstract
Background: The application of normo- and hyperbaric O2 is a common therapy option in various disease patterns. Thereby, the applied O2 affects the whole body, including the blood and its components. This study investigates influences of pressure and oxygen fraction on [...] Read more.
Background: The application of normo- and hyperbaric O2 is a common therapy option in various disease patterns. Thereby, the applied O2 affects the whole body, including the blood and its components. This study investigates influences of pressure and oxygen fraction on human blood plasma, nutrient media, and the functions of neutrophil granulocytes (PMNs). Methods: Neutrophil migration, reactive oxygen species (ROS) production, and NETosis were examined by live cell imaging. The treatment of various matrices (Roswell Park Memorial Institute 1640 medium, Dulbecco’s Modified Eagle’s Medium, H2O, human plasma, and isolated PMNs) with hyperbaric oxygen (HBO) was performed. In addition, the expression of different neutrophil surface epitopes (CD11b, CD62L, CD66b) and the oxidative burst were investigated by flow cytometry (FACS). The application of cold atmospheric plasma (CAP) to normoxic and normobaric culture media served as a positive control. Soluble reaction products such as H2O2, reactive nitrogen species (RNS: NO2 and NO3), and ROS-dependent dihydrorhodamine oxidation were quantified by fluoro- and colorimetric assay kits. Results: Under normobaric normoxia, PMNs migrate slower and shorter in comparison with normobaric hyper- or hypoxic conditions and hyperbaric hyperoxia. The pressure component has less effect on the migration behavior of PMNs than the O2 concentration. Individual PMN cells produce prolonged ROS at normoxic conditions. PMNs showed increased expression of CD11b in normobaric normoxia, lower expression of CD62L in normobaric normoxia, and lower expression of CD66b after HBO and CAP treatment. Treatment with CAP increased the amount of ROS and RNS in common culture media. Conclusions: Hyperbaric and normobaric O2 influences neutrophil functionality and surface epitopes in a measurable way, which may have an impact on disorders with neutrophil involvement. In the context of hyperbaric experiments, especially high amounts of H2O2 in RPMI after hyperbaric oxygen should be taken into account. Therefore, our data support a critical indication for the use of normobaric and hyperbaric oxygen and conscientious and careful handling of oxygen in everyday clinical practice. Full article
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Review

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22 pages, 483 KiB  
Review
Advancing Therapeutic Strategies in Atopic Dermatitis: Emerging Targets and Personalized Approaches
by Yang Lo, Ting-Ting Cheng, Chi-Jung Huang, Yu-Che Cheng and I-Tsu Chyuan
Biomolecules 2025, 15(6), 838; https://doi.org/10.3390/biom15060838 - 8 Jun 2025
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Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder marked by intricate interplay among skin barrier dysfunction, immune dysregulation, and microbial dysbiosis. While therapeutic advancements targeting T helper 2 (Th2) cytokines, such as interleukin (IL)-4 and IL-13, and the Janus kinase/signal transducer and [...] Read more.
Atopic dermatitis (AD) is a chronic inflammatory skin disorder marked by intricate interplay among skin barrier dysfunction, immune dysregulation, and microbial dysbiosis. While therapeutic advancements targeting T helper 2 (Th2) cytokines, such as interleukin (IL)-4 and IL-13, and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway have yielded promising outcomes, a significant proportion of patients still experience inadequate relief, particularly from persistent pruritus. Achieving minimal disease activity remains an unmet clinical priority and a cornerstone of effective AD management. This review provides an in-depth analysis of current therapeutic approaches and integrates findings from recent biologic studies, with a particular focus on innovative strategies under active investigation. These approaches include targeting components of the innate immune system, such as thymic stromal lymphopoietin (TSLP) and IL-1 family cytokines; the adaptive immune system, including OX40-OX40L interactions and Th17- and Th22-related cytokines; and mechanisms associated with pruritus, such as IL-31, histamine receptors, and neurokinin 1 receptor. Emerging insights underscore the transformative potential of personalized therapeutic regimens tailored to the distinct endotypes and severity of AD. Advances in deciphering the pathogenesis of AD are unlocking unprecedented opportunities for precision medicine, offering renewed hope for improved outcomes in this multifaceted and heterogeneous condition. Full article
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23 pages, 1468 KiB  
Review
Pyroptosis: An Accomplice in the Induction of Multisystem Complications Triggered by Obstructive Sleep Apnea
by Jingwen Han, Lisong Ye and Yan Wang
Biomolecules 2024, 14(11), 1349; https://doi.org/10.3390/biom14111349 - 23 Oct 2024
Viewed by 1811
Abstract
Obstructive sleep apnea (OSA) is a common respiratory disorder, primarily characterized by two pathological features: chronic intermittent hypoxia (CIH) and sleep deprivation (SD). OSA has been identified as a risk factor for numerous diseases, and the inflammatory response related to programmed cell necrosis [...] Read more.
Obstructive sleep apnea (OSA) is a common respiratory disorder, primarily characterized by two pathological features: chronic intermittent hypoxia (CIH) and sleep deprivation (SD). OSA has been identified as a risk factor for numerous diseases, and the inflammatory response related to programmed cell necrosis is believed to play a significant role in the occurrence and progression of multisystem damage induced by OSA, with increasing attention being paid to pyroptosis. Recent studies have indicated that OSA can elevate oxidative stress levels in the body, activating the process of pyroptosis within different tissues, ultimately accelerating organ dysfunction. However, the molecular mechanisms of pyroptosis in the multisystem damage induced by OSA remain unclear. Therefore, this review focuses on four major systems that have received concentrated attention in existing research in order to explore the role of pyroptosis in promoting renal diseases, cardiovascular diseases, neurocognitive diseases, and skin diseases in OSA patients. Furthermore, we provide a comprehensive overview of methods for inhibiting pyroptosis at different molecular levels, with the goal of identifying viable targets and therapeutic strategies for addressing OSA-related complications. Full article
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