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Paper Collection: Understanding Immune Systems
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Paper Collection: Understanding Immune Systems

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 2821

Special Issue Editors

Prof. Dr. Sigrun Lange

E-Mail Website
Guest Editor
Pathobiology and Extracellular Vesicles Research Group, School of Life Sciences, University of Westminster, London W1W 6UW, UK
Interests: peptidylarginine deimnases; extracelluar vesicles; regenerative medicine; tissue remodelling; cancer; mucosal immunity; innate immunity; stem cells
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jameel M. Inal

E-Mail Website
Guest Editor
1. School of Life and Medical Sciences, Biosciences Research Group, Extracellular Vesicle Research Unit, University of Hertfordshire, College Lane, Hatfield AL10 9AB, UK
2. School of Human Sciences, Cell Communication in Disease Pathology, London Metropolitan University, 166-220 Holloway Road, London N7 8DB, UK
Interests: immunology; extracellular vesicles; complement system; infectious disease; host-pathogen interactions; vaccinology; virology; microbiology; cancer; intercellular communication; disease mechanisms; biomedicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to collect the state-of-the-art primary research studies, reports, and review articles from international experts and diverse leading groups in the immunology research field. The immune system has multifaceted roles in health and disease, including in developmental processes, during the lifespan, in tissue homeostasis, in evolutionary biology, in host–pathogen interactions and infection, and as a double-edged sword in inflammatory and chronic pathologies. Understanding Immune Systems invites research contributions that further the current understanding in immunology, including from in vitro and in vivo human and comparative animal models.

Prof. Dr. Sigrun Lange
Prof. Dr. Jameel M. Inal
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 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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access semimonthly 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

  • immune mechanisms
  • evolutionary immunology
  • comparative immunology
  • innate immunity
  • adaptive immunity
  • autoimmunity
  • chronic inflammation
  • immune ageing
  • host–pathogen interactions
  • vaccinology
  • regenerative medicine

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

Published Papers (3 papers)

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Research

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20 pages, 3337 KB  
Article
Glycated and Non-Glycated Human Alpha-1 Antitrypsin in Hyperglycemic Wound Healing: In Vivo and In Vitro Models
by Idan Farber, Alon Naumchik, Yosef Istoyler, Melody Zaknoun, Yuval Anav, Lihie Sheffer, Ronen Schuster, Dor Halpern, Vladimir Fridman, Merav Cohen-Lahav, Samuel Cohen, Eli C. Lewis and Eldad Silberstein
Biology 2026, 15(8), 606; https://doi.org/10.3390/biology15080606 - 11 Apr 2026
Viewed by 650
Abstract
Impaired wound healing is a major cause of morbidity among patients with diabetes. Human α1-antitrypsin (hAAT) promotes the resolution of injured tissues. In hyperglycemic conditions, circulating hAAT is likely to undergo glycation, yet it is unknown whether its reparative properties are preserved. We [...] Read more.
Impaired wound healing is a major cause of morbidity among patients with diabetes. Human α1-antitrypsin (hAAT) promotes the resolution of injured tissues. In hyperglycemic conditions, circulating hAAT is likely to undergo glycation, yet it is unknown whether its reparative properties are preserved. We hypothesized that clinical-grade hAAT treatment, but not deliberately glycated hAAT (gly-hAAT), would promote wound repair under hyperglycemic conditions. Mice were rendered hyperglycemic, excisional wounding was performed, and wounds were treated with topical albumin or hAAT every three days. The wound area was assessed, and samples were collected for histology and gene expression analysis. Gly-hAAT was generated from clinical-grade hAAT, after which in vitro RAW 264.7 macrophage responses and re-epithelialization of A549 cells were assessed. Gap closure was further assessed using sera from a human cohort (prospective samples from 10 patients with poorly controlled diabetes at Soroka University Medical Center, Beer-Sheva, Israel, 2018). Group comparisons were performed using one-way ANOVA with Tukey’s post hoc test. hAAT accelerated in vivo wound closure and in vitro A549 cell gap closure, accompanied by an anti-inflammatory IL-1Ra/IL-1β gene expression profile. In contrast, gly-hAAT inhibited normoglycemic mouse wound closure, evoked an inflammatory response in macrophages, and interfered with A549 cell gap closure; concomitant hAAT treatment improved gap closure. Similarly, patient serum inhibited A549 gap closure, and concomitant hAAT treatment improved gap closure. Importantly, inferential statistical analysis was not performed on this outcome due to the small and heterogeneous human cohort. In conclusion, hAAT accelerated wound closure in hyperglycemic mice and in A549 cells, whereas gly-hAAT promoted inflammatory responses and impaired wound closure, a trend reversed by native hAAT. These findings support the concept that glycation undermines the beneficial functions of circulating hAAT and provides a mechanistic insight into the pathophysiology of diabetic wound healing. Further studies are warranted to evaluate clinical-grade hAAT as a potential therapeutic for hyperglycemia-associated impaired wound healing. Full article
(This article belongs to the Special Issue Paper Collection: Understanding Immune Systems)
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13 pages, 4680 KB  
Article
Gestation Regulates Growth Hormone and Its Receptor Expression in Sheep Immune Organs
by Zhouyuan Li, Xiaoxin Ma, Ziwang Du, Jingjing Li, Leying Zhang and Ling Yang
Biology 2025, 14(10), 1318; https://doi.org/10.3390/biology14101318 - 24 Sep 2025
Cited by 1 | Viewed by 1127
Abstract
There are multiple adaptations in maternal physiology, hormones, and immunology during pregnancy. Growth hormone (GH) is not only produced by the pituitary but also secreted by extra-pituitary tissues. In this study, 24 ewes were randomly divided into four groups and mated with either [...] Read more.
There are multiple adaptations in maternal physiology, hormones, and immunology during pregnancy. Growth hormone (GH) is not only produced by the pituitary but also secreted by extra-pituitary tissues. In this study, 24 ewes were randomly divided into four groups and mated with either adult intact rams (pregnant ewes) or a vasectomized ram (nonpregnant ewes), and maternal thymus, lymph node, spleen, and liver were harvested at day 16 of nongestation and at days 13, 16, and 25 of gestation. The specified primers for GH and GH receptor (GHR) were utilized to analyze mRNA expression of GH and GHR using quantitative real-time PCR. Specified anti-GH1 antibody and anti-GHR antibody were used to detect protein expression of GH and GHR using Western blot and immunohistochemical analysis. The results revealed that there were increases in GH and GHR in the maternal spleen, GH in the liver, and GHR in the thymus and lymph nodes, but a downregulation of GH in lymph nodes during early gestation. In addition, early gestation affected GH expression in the thymus and GHR in the liver. In conclusion, it is reported for the first time that early gestation modulates GH and GHR expression in these maternal organs in a tissue-specific manner, which may regulate the function of these immune organs in ewes. Full article
(This article belongs to the Special Issue Paper Collection: Understanding Immune Systems)
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Review

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53 pages, 1146 KB  
Review
Sensory Neuroimmunology: Bidirectional Neuro-Immune Circuits Governing Pain, Itch, Inflammation, and Host Defense at Barrier Surfaces
by Reza Mosaddeghi-Heris, Nasrin Forghani, Negin Safari Dehnavi, Maryam Saberivand, Amir Tahavvori, Sohrab Azin, Niloofar Taheri and Paolo Martelletti
Biology 2026, 15(10), 756; https://doi.org/10.3390/biology15100756 (registering DOI) - 9 May 2026
Viewed by 270
Abstract
Sensory neurons at barrier tissues were once seen as passive detectors of environmental stimuli. However, in the last five years, increasing evidence has challenged this view, redefining these cells as active immune sentinels that directly affect tissue immunity in the skin, lungs, and [...] Read more.
Sensory neurons at barrier tissues were once seen as passive detectors of environmental stimuli. However, in the last five years, increasing evidence has challenged this view, redefining these cells as active immune sentinels that directly affect tissue immunity in the skin, lungs, and gastrointestinal tract. Nociceptors and pruriceptors express various immune-sensing receptors, including Toll-like receptors, cytokine receptors, and alarmin sensors, which allow them to directly detect pathogens, allergens, and tissue damage. When activated, sensory neurons quickly release neuropeptides such as calcitonin gene-related peptide (CGRP), substance P, vasoactive intestinal peptide (VIP), and PACAP (pituitary adenylate cyclase-activating polypeptide), which guide immune cell recruitment, activation, and resolution. Reciprocally, immune-derived mediators, including IL-33, IL-31, thymic stromal lymphopoietin (TSLP), IL-4/IL-13, and TNF-α, modulate neuronal excitability and plasticity, forming bidirectional neuroimmune circuits that control inflammation, host defense, pain, and itch. Landmark studies published in 2024–2025, including neuronal control of gut Treg function and the identification of sensory nerve immune niches, have further refined this framework and revealed tissue-specific circuit specialization. This review synthesizes recent insights from molecular, cellular, and systems levels into the sensory neuroimmune axis, emphasizes its protective versus pathogenic roles, and critically evaluates emerging therapeutic strategies and safety concerns, positioning sensory neuroimmunology as a unifying framework for tissue barrier homeostasis and disease. Full article
(This article belongs to the Special Issue Paper Collection: Understanding Immune Systems)
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