Young Researchers in Immunology

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

Deadline for manuscript submissions: 31 December 2026 | Viewed by 4372

Special Issue Editors


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Guest Editor
Department of Internal Medicine, University of Nebraska Medical Center, Veteran Affairs Medical Center, 4101 Woolworth Ave, R151, Omaha, NE 68105-8080, USA
Interests: hepatitis C, B, HIV, and other viral hepatitis; alcohol-associated liver disease; innate immunity; antigen presentation; proteasome; protein posttranslational modifications; animal models for a hepatitis study; long-acting drugs
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Guest Editor
Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine, Emory University, Atlanta, GA 30322, USA
Interests: lung; liver; HIV; alcohol studies; oxidative stress

Special Issue Information

Dear Colleagues,

This Special Issue aims to highlight the work of early-career researchers in the field of immunology, including postdoctoral fellows and recent PhD graduates. We welcome high-quality original research articles and reviews across all areas of immunology, especially those with innovative or interdisciplinary approaches.

Contributors who obtained their PhD within the past 10 years will also be eligible for consideration for the Biology 2025 Young Investigator Award. The award includes a CHF 1000 prize, a certificate, and a free publication voucher for Biology.

More details can be found here: https://www.mdpi.com/journal/biology/awards/3158

We also encourage submissions from promising PhD students. Co-authored work with senior mentors is welcomed, and the involvement of mentors can further support the development of early-stage researchers.

We look forward to receiving your contributions!

Prof. Dr. Natalia Osna
Dr. Moses New-Aaron
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.

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Published Papers (4 papers)

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Research

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22 pages, 38754 KB  
Article
Phosphatidylserine-Dependent Clearance of Damaged Red Blood Cells by Liver Sinusoidal Endothelial Cells in Alcohol-Related Liver Disease
by Siyuan Li, Chaowen Zheng, Xiaowei Zha, Johannes Mueller, Anne Dropmann, Seddik Hammad, Steven Dooley and Sebastian Mueller
Biology 2026, 15(9), 699; https://doi.org/10.3390/biology15090699 - 29 Apr 2026
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Abstract
Alcohol-related liver disease (ALD) and ALD-related mortality are associated with hemolysis, increased erythrophagocytosis, and disturbed iron homeostasis. While macrophage-mediated erythrophagocytosis is well established, we investigated the contribution of liver sinusoidal endothelial cells (LSECs) to handling oxidatively damaged or ethanol-primed red blood cells (RBCs) [...] Read more.
Alcohol-related liver disease (ALD) and ALD-related mortality are associated with hemolysis, increased erythrophagocytosis, and disturbed iron homeostasis. While macrophage-mediated erythrophagocytosis is well established, we investigated the contribution of liver sinusoidal endothelial cells (LSECs) to handling oxidatively damaged or ethanol-primed red blood cells (RBCs) in ALD. Live-cell imaging demonstrated that damaged RBCs were rapidly taken up by SK-HEP1 cells, an endothelial cell line with LSEC-like characteristics, and RBC uptake was associated with induction of heme oxygenase-1 (HO-1) and activation of its upstream regulator Nrf2. siRNA-mediated knockdown of the scavenger receptor Stabilin-1 attenuated RBC-induced HO-1 expression, supporting a role for Stabilin-1 in efferocytic signaling. Exposure of RBCs to ethanol concentrations as low as 25 mM induced phosphatidylserine externalization and rendered erythrocytes efferocytosis-competent. Lysed RBCs and free hemin elicited comparable oxidative stress responses. In murine models of hemolysis and chronic ethanol feeding, hemoglobin-derived signals were detected within sinusoidal structures showing a diffuse CD206-positive distribution pattern consistent with the sinusoidal scavenger compartment. Similar signals were observed in sinusoidal endothelial regions in human heavy drinkers with clinical signs of hemolysis. Together, these data suggest that LSECs may represent an additional component of RBC clearance in ALD, alongside macrophages and hepatocytes, with implications for hepatic iron handling. Full article
(This article belongs to the Special Issue Young Researchers in Immunology)
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17 pages, 3112 KB  
Article
Chronic Alcohol Consumption Reprograms Osteoclast Lineage Communications to Promote Osteoclastogenesis
by Hami Hemati, Brianna M. Doratt and Ilhem Messaoudi
Biology 2026, 15(7), 527; https://doi.org/10.3390/biology15070527 - 26 Mar 2026
Viewed by 528
Abstract
Chronic alcohol consumption increases the risk of osteoporosis and fracture by disrupting bone remodeling, in part by enhancing osteoclastogenesis. However, the cellular mechanisms underlying this process remain incompletely defined. We analyzed scRNA-seq data from osteoclasts differentiated in vitro from bone marrow mononuclear cells [...] Read more.
Chronic alcohol consumption increases the risk of osteoporosis and fracture by disrupting bone remodeling, in part by enhancing osteoclastogenesis. However, the cellular mechanisms underlying this process remain incompletely defined. We analyzed scRNA-seq data from osteoclasts differentiated in vitro from bone marrow mononuclear cells obtained from macaques following 12 months of chronic ethanol or isocaloric control solution consumption. Module scoring, trajectory inference with generalized additive modeling (tradeSeq), and CellChat-based analyses of intercellular communication were applied to uncover ethanol-induced changes in metabolic reprogramming, lineage progression, and signaling network dynamics. Module scoring indicated metabolic reprogramming toward oxidative phosphorylation, with reduced glycolytic, migratory, and phagocytic activities. Pseudotime analysis revealed accelerated osteoclast lineage commitment, broader intermediate differentiation states, and stabilization of mature osteoclasts. CellChat analysis showed globally amplified intercellular signaling, with mature osteoclasts functioning as dominant communication hubs sustained by autocrine feedback. Together, chronic alcohol consumption rewired osteoclastogenesis through early fate priming, metabolic adaptation, and hierarchical remodeling of intercellular communication, promoting enhanced osteoclastogenesis. These findings provide mechanistic insight into alcohol-induced bone pathology and highlight potential targets for therapeutic intervention. Full article
(This article belongs to the Special Issue Young Researchers in Immunology)
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18 pages, 8853 KB  
Article
Clinical Serum-Anchored Computational Design Pipeline for a Broad-Spectrum Influenza Multi-Epitope mRNA Vaccine
by Lifang Yuan, Zhiyao Ouyang, Yifan Zhao, Rongjun Bi, Yanjing Wu, Xu Li, Yingrui Li, Jiaping Song, Wei Li, Mingchen Yan, Simin Wen, Huanle Luo, Tian Bai, Yuelong Shu and Yongkun Chen
Biology 2026, 15(4), 357; https://doi.org/10.3390/biology15040357 - 19 Feb 2026
Cited by 1 | Viewed by 887
Abstract
Influenza’s pandemic threat is driven by antigenic drift, which limits the efficacy of conventional vaccines. To address this challenge, we established a clinical serum-anchored computational design pipeline for a broad-spectrum multi-epitope mRNA vaccine (MEMV), bridging the gap between pure in silico design and [...] Read more.
Influenza’s pandemic threat is driven by antigenic drift, which limits the efficacy of conventional vaccines. To address this challenge, we established a clinical serum-anchored computational design pipeline for a broad-spectrum multi-epitope mRNA vaccine (MEMV), bridging the gap between pure in silico design and clinical applicability. Using 36 longitudinal sera (d0/d28/d365) from 12 well-characterized human cohorts (6 vaccine recipients and 6 influenza patients) and high-density antibody-peptide microarrays, we empirically identified 12 immunodominant B-cell linear epitopes from the nucleoprotein (NP) of influenza A (H1N1/H3N2) and B viruses. These experimentally validated epitopes were combined with in silico-predicted conserved helper T-lymphocyte (HTL)/cytotoxic T-lymphocyte (CTL) epitopes (from NP/HA/NA) to construct MEMVs candidates, ensuring high antigenicity, non-toxicity, and 95.63% global HLA coverage. Molecular docking and 100 ns molecular dynamics (MD) simulations confirmed favorable conformational compatibility between MEMVs and Toll-like receptor 3 (TLR3) in silico immunization via C-ImmSim predicted robust B/T-cell responses and protective cytokine (IFN-γ/IL-10) production. Collectively, this pipeline shortens the preliminary design cycle for influenza vaccines, provides a standard epitope-combination strategy, and offers direct targets for follow-up in vitro/in vivo experiments. Full article
(This article belongs to the Special Issue Young Researchers in Immunology)
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Review

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22 pages, 1130 KB  
Review
Hepatic Macrophages in Chronic Hepatitis B: Balancing Immunity and Pathology
by Anup S. Pathania, Sajad A. Bhat, Lukman A. Adepoju, Kusum K. Kharbanda and Natalia A. Osna
Biology 2026, 15(1), 76; https://doi.org/10.3390/biology15010076 - 31 Dec 2025
Viewed by 1421
Abstract
Chronic HBV infection remains a global health challenge, driving liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Liver injury is primarily mediated by host immune responses rather than direct viral cytotoxicity. Macrophages, including Kupffer cells, play dual roles in antiviral defense and disease progression. [...] Read more.
Chronic HBV infection remains a global health challenge, driving liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Liver injury is primarily mediated by host immune responses rather than direct viral cytotoxicity. Macrophages, including Kupffer cells, play dual roles in antiviral defense and disease progression. HBV skews macrophages toward an M2-like, immunosuppressive phenotype, promoting viral persistence and fibrogenesis via cytokines such as Interleukin (IL)-10 and Transforming growth factor-beta (TGF-β). Therapeutic strategies targeting macrophage polarization, including Toll-like receptor (TLR) agonists, immune checkpoint inhibitors, and nanoparticle-based systems, are under investigation. Addressing macrophage heterogeneity and the immunosuppressive hepatic microenvironment using advanced models is essential. Modulating macrophages offers a promising avenue to control HBV, restore immune balance, and mitigate liver injury. This review highlights the central role of macrophages in chronic HBV infection and explores emerging therapeutic strategies. Full article
(This article belongs to the Special Issue Young Researchers in Immunology)
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