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New Insights into Immune Dysregulation Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 30 January 2025 | Viewed by 515

Special Issue Editor


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Guest Editor
Centro Tettamanti, Fondazione IRCCS San Gerardo dei Tintori, Monza, Italy
Interests: inborn errors of immunity; primary immunodeficiencies; clinical immunology

Special Issue Information

Dear Colleagues,

The Special Issue entitled "New Insights into Immune Dysregulation Disorders" in the International Journal of Molecular Sciences will present groundbreaking research on the molecular mechanisms of immune dysregulation disorders, encompassing autoimmune conditions, primary immunodeficiencies, and autoinflammatory disorders. It will highlight advancements in understanding specific genes, signalling pathways, and molecular interactions in the pathogenesis of these disorders. Advanced techniques, such as next-generation sequencing, CRISPR gene editing, and omics (proteomics, lipidomics, and metabolomics), will be utilised to uncover new molecular targets and biomarkers for early diagnosis and treatment. This Special Issue will discuss how this knowledge will lead to precision medicine approaches, including targeted biologics and gene therapies, aimed at restoring immune balance. By focusing on the molecular level of these conditions, this Special Issue aims to pave the way for novel therapeutic interventions that could significantly improve patient outcomes.

Dr. Francesco Saettini
Guest Editor

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Keywords

  • immune dysregulation disorders
  • autoimmune conditions
  • primary immunodeficiencies
  • autoinflammatory disorders

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Published Papers (1 paper)

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Research

18 pages, 3771 KiB  
Article
Neutrophil Diversity (Immature, Aged, and Low-Density Neutrophils) and Functional Plasticity: Possible Impacts of Iron Overload in β-Thalassemia
by Kritsanawan Sae-Khow, Awirut Charoensappakit and Asada Leelahavanichkul
Int. J. Mol. Sci. 2024, 25(19), 10651; https://doi.org/10.3390/ijms251910651 - 3 Oct 2024
Viewed by 371
Abstract
Neutrophil dysfunction is a form of immune suppression in patients with β-thalassemia (Beta-thal), although data on this are limited. In this study, blood from patients and healthy volunteers was analyzed. Flow cytometry analysis demonstrated an increase in immature neutrophils (CD16− CD62L+) and aged [...] Read more.
Neutrophil dysfunction is a form of immune suppression in patients with β-thalassemia (Beta-thal), although data on this are limited. In this study, blood from patients and healthy volunteers was analyzed. Flow cytometry analysis demonstrated an increase in immature neutrophils (CD16− CD62L+) and aged (senescent) neutrophils (CD16+ CD62L−) in Beta-thal patients compared to healthy volunteers. The Beta-thal neutrophils demonstrated less prominent chemotaxis and phagocytosis than healthy neutrophils at the baseline. With phorbol myristate acetate (PMA) or lipopolysaccharide (LPS) stimulations, some of the indicators, including the flow cytometry markers (CD11b, CD62L, CD66b, CD63, apoptosis, and reactive oxygen species) and neutrophil extracellular traps (NETs; detected by anti-citrullinated histone 3 immunofluorescence), were lower than the control. Additionally, low-density neutrophils (LDNs), which are found in the peripheral blood mononuclear cell (PBMC) fraction, were observed in Beta-thal patients but not in the control group. The expression of CD11b, CD66b, CD63, arginase I, and ROS in LDNs was higher than the regular normal-density neutrophils (NDNs). The proliferation rate of CD3+ T cells isolated from the PBMC fraction of healthy volunteers was higher than that of the cells from patients with Beta-thal. The incubation of red blood cell (RBC) lysate plus ferric ions with healthy NDNs transformed the NDNs into the aged neutrophils (decreased CD62L) and LDNs. In conclusion, iron overload induces neutrophil diversity along with some dysfunctions. Full article
(This article belongs to the Special Issue New Insights into Immune Dysregulation Disorders)
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