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Molecular Basis of Autoimmune Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 400

Special Issue Editor


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Guest Editor
1. Vaccine and Infectious Disease Division, Frech Hutchinsion Cancer Center, Seattle, WA, USA
2. Kennedy Institute of Rheumatology, University of Oxford, Old Road Campus, Roosevelt Drive, Headington, Oxford, UK
Interests: auto-immunity; antibody discovery; B-cell biology; multi-omics

Special Issue Information

Dear Colleagues,

Autoimmune diseases arise from complex interactions between genetic, epigenetic, and environmental factors, leading to immune system dysregulation and self-reactivity. Recent advancements in molecular biology have significantly improved our understanding of the mechanisms underlying autoimmunity, including the roles of immune checkpoints, cytokine signaling, genetic predisposition, and epigenetic modifications. Identifying the molecular markers and pathways associated with autoimmune disorders is essential in developing targeted therapeutic strategies and improving diagnostic precision.

This Special Issue, “Molecular Basis of Autoimmune Diseases”, will explore the latest discoveries around the molecular mechanisms driving autoimmune diseases. We welcome original research articles and reviews covering topics such as immune system dysfunction, novel biomarkers, gene–environment interactions, therapeutic advancements, and emerging technologies in autoimmune disease research. Studies incorporating genomics, transcriptomics, proteomics, and systems biology approaches are particularly encouraged.

By bringing together cutting-edge research, this Special Issue will provide insights into disease pathogenesis, identify potential intervention strategies, and highlight novel therapeutic targets to improve patient outcomes.

Dr. Ranjeet Singh Mahla
Guest Editor

Manuscript Submission Information

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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. Current Issues in Molecular Biology 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 2200 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

  • autoimmune diseases
  • immune regulation
  • molecular mechanisms
  • genetic predisposition
  • epigenetics
  • cytokines
  • biomarkers
  • immune checkpoints
  • targeted therapies
  • genomics
  • transcriptomics
  • proteomics
  • systems biology
  • inflammation
  • immune tolerance

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Published Papers (1 paper)

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Research

10 pages, 836 KiB  
Article
IFN-γ +874 T/A Is Associated with High Levels of Sera CPK in Patients with Inflammatory Myopathies
by Mónica Vázquez-Del Mercado, Beatriz Teresita Martín-Márquez, Erika Aurora Martínez-García and Marcelo Heron Petri
Curr. Issues Mol. Biol. 2025, 47(7), 492; https://doi.org/10.3390/cimb47070492 - 27 Jun 2025
Viewed by 274
Abstract
Aim of the study: Idiopathic inflammatory myopathies (IIM) are autoimmune diseases with a low prevalence and incidence worldwide. The levels of IFN-γ production by T-lymphocytes are related to disease activity. IFN-γ +874 T/A (rs2430561) has been shown to alter the serum levels of [...] Read more.
Aim of the study: Idiopathic inflammatory myopathies (IIM) are autoimmune diseases with a low prevalence and incidence worldwide. The levels of IFN-γ production by T-lymphocytes are related to disease activity. IFN-γ +874 T/A (rs2430561) has been shown to alter the serum levels of IFN-γ in different pathologies. The aim of this work is to explore the role of IFN-γ +874 T/A polymorphism in IIM. Methods: Using a specific sequence primer-polymerase chain reaction (SSP-PCR), the genotype was defined for normal healthy controls (HC) and patients with IIM. Markers of muscle damage, clinical features and treatment were collected from chart at the time of diagnosis and at recruitment point. All the data were analyzed by demographic characteristics, genotype, type of IIM, treatment, clinical features, and enzymatic levels. Results: No association was found comparing the genotypes or alleles of the IIM patients vs. HC. On the other hand, the TT genotype, previously described as a high producer of INF γ, showed higher levels of CPK at diagnosis in IIM patients, whereas females at diagnosis and males in remission presented higher levels. Conclusions: Even with a limited number of patients due to the rarity of this disease, no association was found between the disease development. Further, the TT genotype promoted muscle damage due to CPK elevation in the sera compared to the TA/AA genotype in patients with IIM. This could be genetic evidence of the impact of IFN-γ in the disease activity of IIM patients. A larger cohort is needed to confirm these results. Full article
(This article belongs to the Special Issue Molecular Basis of Autoimmune Diseases)
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