Transcription Factors in Hematopoiesis and Immunity: From Development to Therapeutic Targeting

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

Deadline for manuscript submissions: 3 May 2026 | Viewed by 1811

Special Issue Editor


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Guest Editor
Immunology and Molecular Hematology Group, Peninsula Medical School, University of Plymouth, Plymouth PL6 8BU, UK
Interests: hematopoiesis; anemia; cancer; cytokine signaling; transcription factors; immunity

Special Issue Information

Dear Colleagues,

Biomolecules invites submissions to a Special Issue focused on the transcriptional regulation of hematopoiesis and its impact on immune system functioning in health and disease.

It has been established that various types of transcription factors control key stages of the hematopoietic stem cell cycle as well as the entirety of hematopoietic lineage cell development. While these factors usually facilitate hematopoiesis and provide immunity against a range of diseases, alterations in terms of deficiency or overactivity can lead to severe consequences ranging from immunodeficiency to cancer. Although lineage commitment, proliferation, and differentiation are the common processes for all hematopoietic lineage cells, these activities are regulated by distinct transcription factors via precisely controlled signaling and epigenetic mechanisms in every lineage. Although huge progress has been made in understanding the fundamental regulation of various hematopoietic cell functions in immunity, an integrated picture of the interaction and counteraction of the transcription factors maintaining the balance between health and disease is yet to emerge.

This Special Issue invites submissions that focus on novel understandings of the underlying transcriptional mechanisms of hematopoietic/immune lineage cell development and the opportunities and challenges to target lineage-specific transcription factors to control associated disease pathogenesis.

Dr. Amiya Kumar Patra
Guest Editor

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Keywords

  • transcription factors
  • immune regulation
  • epigenetics
  • cytokines and chemokines
  • molecular interaction
  • immunodeficiency
  • allergy
  • leukemia and lymphoma
  • small molecule inhibitors
  • hematopoietic disorders

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Published Papers (2 papers)

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Research

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16 pages, 5174 KB  
Article
Glucocorticoids Induce an Opposite Metabolic Switch in Human Monocytes Contingent upon Their Polarization
by Elisa Peruzzi, Sophia Heidenreich, Lucas Klaus, Angela Boshnakovska, Agathe Amouret, Tobias Legler, Sybille D. Reichardt, Fred Lühder and Holger M. Reichardt
Biomolecules 2025, 15(10), 1422; https://doi.org/10.3390/biom15101422 - 7 Oct 2025
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Abstract
Background: Monocytes can commit to different phenotypes associated with specific features required in inflammation and homeostasis. Classical and alternative activation are two extremes of monocyte polarization and are both influenced by glucocorticoids (GCs). Methods: Human monocytes were sorted from the blood of healthy [...] Read more.
Background: Monocytes can commit to different phenotypes associated with specific features required in inflammation and homeostasis. Classical and alternative activation are two extremes of monocyte polarization and are both influenced by glucocorticoids (GCs). Methods: Human monocytes were sorted from the blood of healthy individuals and activated with LPS or IL-4 and IL-13, either in the absence or presence of dexamethasone (Dex). Metabolic adjustments were analyzed using Seahorse stress tests, SCENITH, and RT-qPCR. Results: LPS enhanced glycolysis and also, to a lesser extent, oxidative phosphorylation (OXPHOS), whereas addition of Dex induced a metabolic switch in favor of the latter. In contrast, activation of monocytes with IL-4 and IL-13 exclusively stimulated OXPHOS, which was suppressed by concomitant Dex treatment. The glycolytic function of monocytes matched alterations in gene expression of glucose transporters and metabolic enzymes, which were upregulated by LPS and inhibited by Dex via interference with the mTORC1 pathway but remained unaltered in response to IL-4 and IL-13. Although the dependency of classically and alternatively activated monocytes on OXPHOS and glucose usage markedly differed, modulation by GCs was limited to the latter polarization state. Conclusions: Our findings unravel a highly selective regulation of human monocyte energy metabolism by different activating stimuli as well as by GCs. Full article
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Review

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25 pages, 1697 KB  
Review
Critical Evaluation of the Role of Transcription Factor RAR-Orphan Receptor-γt in the Development of Chronic Inflammatory Dermatological Diseases: A Promising Therapeutic Target
by Anik Pramanik, Pallabi Mondal and Sankar Bhattacharyya
Biomolecules 2025, 15(11), 1543; https://doi.org/10.3390/biom15111543 - 2 Nov 2025
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Abstract
Nuclear receptors (NRs) are transcription factors regulated by ligands that direct metabolism, development, and immunity. The NR superfamily constitutes a principal category of pharmacological targets for human ailments. Retinoic acid receptor-related orphan receptors (RORs) α, β, and γ are part of the nuclear [...] Read more.
Nuclear receptors (NRs) are transcription factors regulated by ligands that direct metabolism, development, and immunity. The NR superfamily constitutes a principal category of pharmacological targets for human ailments. Retinoic acid receptor-related orphan receptors (RORs) α, β, and γ are part of the nuclear receptor superfamily. They are nevertheless classified as “orphan” receptors due to the contentious nature of identifying their endogenous ligands. RORγ nuclear receptor protein further consists of two isoforms, namely RORγ1 and RORγ2 or RORγt. RORγt is largely found in immune cells and has been primarily associated with chronic inflammatory conditions. The expression of STAT3 is a major driver of Th17 differentiation and induces RORγt expression through the JAK-STAT pathway. Type 3 innate lymphoid cells (ILC3s), Th17 cells, and γδT cells express RORγt, the master transcription regulator for the pro-inflammatory cytokine interleukin IL-17. In chronic inflammatory skin disorders, a significant increase in IL-17 has been observed, which plays a key role in both immune cell recruitment to the site of inflammation and the propagation of tissue damage. In this review, we will discuss how RORγt regulates IL-17-driven inflammation and explore potential strategies to target the RORγt-IL-17 axis as a viable therapeutic intervention in chronic inflammatory skin disorders. Full article
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