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Cells
Special Issues
Cellular and Molecular Mechanisms in Immune Regulation—Second Edition
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Cellular and Molecular Mechanisms in Immune Regulation—Second Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 1159

Special Issue Editors

Dr. Fábio Rinaldo Santori

E-Mail Website
Guest Editor
Center for Molecular Medicine, University of Georgia, Athens, GA, USA
Interests: nuclear receptors; immunology; T cell biology; stem cells; transcriptional regulation
Special Issues, Collections and Topics in MDPI journals
Dr. Natalia B. Ivanova

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Center for Molecular Medicine, University of Georgia, Athens, GA, USA
Interests: epigenetics; stem cells; transcriptional regulation; hematopoiesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following the successful completion of the first edition of our Special Issue, titled “Cellular and Molecular Mechanisms in Immune Regulation”, we are pleased to announce the launch of its second edition.

Vaccines and immunotherapies for infectious diseases and cancer are key components of modern medicine. The next generation of immune therapies will come from a better understanding of how the immune system interacts and how it is regulated by local tissues. In this Special Issue of Cells, entitled “Cellular and Molecular Mechanisms in Immune Regulation—Second Edition”, we will explore the following topics: the regulation of T cell maintenance in the periphery and formation of immunological memory; the role of innate immune cells and fibroblasts in wound healing, cancer, and autoimmune diseases; the regulation of inflammation and the immune response by nerve cells; and the role of innate lymphoid cells (ILCs) in the development of lymphoid tissues. We also welcome manuscripts showing how these processes can be manipulated by biological therapies, monoclonal antibodies, and CAR T cells for the treatment of infections, cancers, and autoimmune diseases.

We look forward to your contributions.

Dr. Fábio Rinaldo Santori
Dr. Natalia B. Ivanova
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. Cells 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

  • innate immunity
  • dendritic cells
  • macrophages
  • T cells
  • B cells
  • cytokines
  • immunotherapy

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Published Papers (2 papers)

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17 pages, 2618 KB  
Article
Alterations in Resident Immune Cells in Prenatal Trisomy 21 Lungs
by Andrew Frauenpreis, Soumyaroop Bhattacharya, Randa Belgacemi, Pauline Sokolskiy, Gail Deutsch, Nicholas Jendzjowsky, Ian A. Glass, Thomas J. Mariani, Denise Al Alam and Soula Danopoulos
Cells 2025, 14(23), 1866; https://doi.org/10.3390/cells14231866 - 26 Nov 2025
Viewed by 330
Abstract
Respiratory tract infections (RTIs) are amongst the leading causes of hospitalizations in children with Down syndrome (DS). Their elevated susceptibility likely stems from structural differences in the airways and immune system abnormalities. The aim of this study was to characterize immune cells in [...] Read more.
Respiratory tract infections (RTIs) are amongst the leading causes of hospitalizations in children with Down syndrome (DS). Their elevated susceptibility likely stems from structural differences in the airways and immune system abnormalities. The aim of this study was to characterize immune cells in prenatal Trisomy 21 (T21) lungs, potentially explaining vulnerability to RTIs. Single-cell RNA sequencing was used to profile immune cells in prenatal T21 (n = 5) and non-T21 (n = 4) prenatal lungs. Spatial phenotypes were assessed via fluorescent in situ hybridization and immunofluorescent staining on prenatal lung tissue sections. Gene expression analysis was also performed on isolated immune cells from lung single-cell suspensions. Several major immune cell populations were identified. A total of 84 DEGs were identified in at least 1 of the 14 different clusters. A significant decrease in the percentage of B cells was observed in T21 lungs (FDR = 0.0037, * p < 0.05). Furthermore, qRT-PCR demonstrated B cell markers were significantly decreased in T21, including those associated with B cell maturation (* p < 0.05 and ** p < 0.01). Several of these markers were also decreased at the protein level (i.e., CD20 and CD38; * p < 0.05 and ** p < 0.01). Our data demonstrate changes in the T21 pulmonary immune system in utero, primarily within the B cell population, which may contribute to the increased susceptibility to RTIs observed in children with DS. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Immune Regulation—Second Edition)
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20 pages, 4762 KB  
Article
TNFR1 Suppression by XPro1595 Reduces Peripheral Neuropathies Associated with Perineural Invasion in Female Mice
by Morgan Zhang, Naijiang Liu, Kesava Asam, Charles Meng, Bradley Aouizerat and Yi Ye
Cells 2025, 14(22), 1749; https://doi.org/10.3390/cells14221749 - 7 Nov 2025
Viewed by 565
Abstract
Perineural invasion (PNI), defined by cancer spreading or invading into the nerve, links to severe pain, recurrence, and poor prognosis. PNI contributes to nerve damage, Schwann cell activation, and sensory neuron dysfunction. Soluble tumor necrosis factor α (solTNFα) binds to TNFR1 to drive [...] Read more.
Perineural invasion (PNI), defined by cancer spreading or invading into the nerve, links to severe pain, recurrence, and poor prognosis. PNI contributes to nerve damage, Schwann cell activation, and sensory neuron dysfunction. Soluble tumor necrosis factor α (solTNFα) binds to TNFR1 to drive inflammation and nerve injury, playing a key role in cancer progression and pain. This study, using a mouse sciatic nerve PNI model, explored whether blocking solTNFα-TNFR1 signaling via TNFR1 knockout or pharmacological inhibition by XPro1595 could reduce PNI-associated pain. Data showed that XPro1595, but not TNFR1 knockout, reduced tumor burden, alleviated mechanical allodynia, and improved muscle function and locomotion, primarily in females. Histological analysis in females showed that XPro1595 increased the number of myelin and dendritic cells while reducing axonal damage that resulted from PNI. In the tumor zone outside the nerve truck, XPro1595 reduced T cell and increased macrophage and dendritic cell numbers. Transcriptomic analysis revealed that XPro1595 in females with PNI upregulated mitochondrial, myelination, motor function, and immune regulation gene pathways while it downregulated inflammatory, extracellular matrix, and tumor progression pathways. Overall, we demonstrated that XPro1595 exhibited antitumor, neuroprotective, and analgesic properties in female mice, likely by promoting neuronal regeneration and mitochondrial function, while reducing inflammation and extracellular remodeling. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Immune Regulation—Second Edition)
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