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Biomedicines
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Advances in Immune Cell Biology: Insights from Molecular Perspectives
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Advances in Immune Cell Biology: Insights from Molecular Perspectives

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 1787

Special Issue Editor

Dr. Paolo Fagone

E-Mail Website
Guest Editor
Department of Biomedical and Biotechnological Sciences, University of Catania, Via Santa Sofia, 97, 95123 Catania, Italy
Interests: immunotherapy; oncology; neuroimmunology; autoimmunity; bioinformatics and computational biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, immune cell biology has undergone significant advancements, shedding light on the mechanisms that regulate the behavior of immune cells in both health and disease. This dynamic research field investigates the complex molecular pathways orchestrating immune cell maturation, differentiation, activation, and proliferation, offering valuable insights into the etiology of autoimmune, immunoinflammatory, and hematological disorders. This Special Issue of Biomedicine invites authors to contribute original research papers and reviews on the molecular mechanisms underlying autoimmune, immunoinflammatory, and hematological disorders. This issue explores the molecular mechanisms that enable the differentiation of immune cells from precursor cells, their polarization into effector cells, and the functioning of the regulatory signaling pathways that shape immune responses. Additionally, it focuses on the processes of immune memory formation and on the genetic and molecular alterations leading to the transformation of normal immune cells into neoplasms. The primary goal is to expand our understanding of these diseases, paving the way for more targeted diagnostic and therapeutic approaches.

Dr. Paolo Fagone
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 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. 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

  • immune cell biology
  • cell signaling cascades
  • autoimmune disorders
  • immunoinflammatory pathways
  • hematological disorders

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Published Papers (2 papers)

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Research

12 pages, 1252 KB  
Article
Transcriptional Control of TSPAN32 in T-ALL Reveals Interplay Between TAL1 and NOTCH1
by Grazia Scuderi, Antonio Arcidiacono, Eugenio Cavalli, Maria Sofia Basile, Antonella Nardo, Ferdinando Nicoletti and Paolo Fagone
Biomedicines 2025, 13(9), 2090; https://doi.org/10.3390/biomedicines13092090 - 27 Aug 2025
Viewed by 367
Abstract
Background: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of immature T cells, driven by dysregulated transcriptional networks and oncogenic signaling pathways. Here, we present the first comprehensive analysis of the expression and regulation of TSPAN32, a tetraspanin implicated in lymphocyte homeostasis, [...] Read more.
Background: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of immature T cells, driven by dysregulated transcriptional networks and oncogenic signaling pathways. Here, we present the first comprehensive analysis of the expression and regulation of TSPAN32, a tetraspanin implicated in lymphocyte homeostasis, in T-ALL. Methods: Transcriptomic data from the Leukemia MILE study (GSE13159) were analyzed to assess TSPAN32 expression across leukemic subtypes. Gene Set Enrichment Analysis (GSEA) was performed to explore biological pathways associated with TSPAN32-correlated genes. For mechanistic validation, HPB-ALL cells were used as a model, with NOTCH signaling inhibited by γ-secretase inhibitor (GSI) treatment and TAL1–LMO1 overexpression induced through doxycycline-inducible lentiviral vectors. Gene expression changes were quantified by RT-qPCR. Results: TSPAN32 was frequently downregulated in T-ALL compared to healthy bone marrow, although expression was retained in a subset of cases. GSEA revealed that TSPAN32-correlated genes were inversely associated with cell cycle–related programs, consistent with its established role as a negative regulator of T cell proliferation. Mechanistically, TAL1–LMO1 overexpression strongly induced TSPAN32, while GSI-mediated NOTCH inhibition partially reactivated its expression. Interestingly, GSI treatment also increased TAL1 levels despite downregulating LMO1. Conversely, TAL1–LMO1 overexpression suppressed NOTCH1 and NOTCH3, highlighting a reciprocal regulatory interplay between NOTCH and TAL1/LMO1 oncogenic circuits that shapes TSPAN32 expression dynamics in T-ALL. Conclusions: This study identifies TSPAN32 as a novel transcriptional target under the influence of key leukemogenic pathways and suggests its potential role as a modulator of leukemic T cell proliferation, with implications for therapeutic strategies targeting TAL1 and NOTCH signaling. Full article
(This article belongs to the Special Issue Advances in Immune Cell Biology: Insights from Molecular Perspectives)
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16 pages, 3251 KB  
Article
Histological Alterations and Interferon-Gamma and AKT-mTOR Expression in an Experimental Model of Achilles Tendinopathy—A Comparison of Stem Cell and Amniotic Membrane Treatment
by Guilherme Vieira Cavalcante, Rosangela Fedato, Lucia de Noronha, Seigo Nagashima, Ana Paula Camargo Martins, Márcia Olandoski, Ricardo Pinho, Aline Takejima, Rossana Simeoni, Julio Cesar Francisco and Luiz César Guarita-Souza
Biomedicines 2025, 13(2), 525; https://doi.org/10.3390/biomedicines13020525 - 19 Feb 2025
Viewed by 855
Abstract
Achilles tendon injuries are extremely common and have a significant impact on the physical and mental health of individuals. Both conservative and surgical treatments have unsatisfactory results. The search for new therapeutic tools, using cell therapies with stem cells (SC) and biological tissues, [...] Read more.
Achilles tendon injuries are extremely common and have a significant impact on the physical and mental health of individuals. Both conservative and surgical treatments have unsatisfactory results. The search for new therapeutic tools, using cell therapies with stem cells (SC) and biological tissues, such as amniotic membranes (AM), has proved useful for the regeneration of injured tendons. Background/Objectives: This research was carried out to assess the capacity of tissue repair in animal models of Achilles tendinopathy, in which rats were submitted to complete sections of the tendon, and the effects of using bone marrow SC and/or AM graft are evaluated. Methods: Thirty-seven Wistar rats, submitted to complete surgical section of the Achilles tendon and subsequent tenorrhaphy, were randomized into four groups: Control Group (CG), received saline solution; SC Group (SCG) received an injection of SC infiltrated directly into the tendon; AM Group (AMG), the tendon was covered with an AM graft; SC + AM Group (SC+AMG), has been treated with an AM graft and SC local injection. Six weeks later, the Achilles tendons were evaluated using a histological score and immunohistochemical pro-healing markers such as Interferon-γ, AKT, and mTOR. Results: There were no differences between morphometric histological when evaluating the Achilles tendons of the samples. No significant differences were found regarding the expression of AKT-2 and mTOR markers between the study groups. The main finding was the presence of a higher concentration of Interferon-γ in the group treated with SC and AM. Conclusions: The isolated use of SC, AM, or the combination of SC-AM did not produce significant changes in tendon healing when the histological score was evaluated. Similarly, no difference was observed in the expression of AKT-2 and mTOR markers. An increase in the expression of Interferon-γ was observed in SC+AMG. This suggests that such therapies may be potentially beneficial for the regeneration of injured tendons. However, as tendon repair mechanisms are very complex, further studies should be carried out to verify the benefits of the tendon structure and function. Full article
(This article belongs to the Special Issue Advances in Immune Cell Biology: Insights from Molecular Perspectives)
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