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Molecular Insights into Autoimmune Diseases

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: 20 June 2025 | Viewed by 1718

Special Issue Editors


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Guest Editor
Department of Health Sciences, Università del Piemonte Orientale (UPO), 28100 Novara, Italy
Interests: biomaterials; nanomaterials; regenerative medicine; vitamin D; extracellular matrix; inflammatory and rheumatic diseases; cardiovascular diseases; translational research
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Internal Medicine Unit, Department of Translational Medicine, Università del Piemonte Orientale, 28100 Novara, Italy
Interests: multiple sclerosis; autoimmune diseases; anti-rheumatic drug therapy; osteoporosis; hypovitaminosis D; chronic inflammatory demyelinating polyneuropathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autoimmune diseases are clinical entities characterized by etherogeneous clinical manifestation, the pathogenesis of which relies on environmental and genetic determinants that determine the loss of immunological tolerance, finally leading to a dysregulated immune response. One relevant feature of these conditions is the production of autoantibodies directed against self antigens. These pathological autoantibodies, which are the hallmark of autoimmune diseases, are known to be involved in disease pathogensesis in different ways, as they can directly damage the host tissues or induce an aberrant activation of the intracellular signaling pathways. Autoimmune diseases have no predefined targets but can affect a wide range of human tissues, such as the skin, the muscles, the nerves, the joints, and the endocrine glands. In all cases, autoantibody production eventually results in tissue damage and severe inflammation. Due to the sustained inflamatory response that accompanies tissue damage, the most conventional therapeutic approach is represented by anti-inflammatory drugs. However, it is worth noting that in the last decades, many targeted therapies, such as non conventional diesease modifying drugs and biologics, have started to emerge.

The aim of this Special Issue is to collect updated information about the molecular mechanisms involved in autoimmune disease pathophysiology. Moreover, contributions dealing with the identification and validation of novel biomarkers as well as new therapeutic targets are welcome. Last but not least, reports focused on the molecular basis of available or experimental therapeutic approaches are encouraged. To reach this goal, we encourage the submission of both comprehensive reviews and original articles offering original insights into the molecular aspects of autoimmune disease pathophysiology and treatment.

Dr. Manuela Rizzi
Dr. Pier Paolo Sainaghi
Guest Editors

Manuscript Submission Information

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Keywords

  • autoimmune diseases
  • autoantibodies
  • biomarkers
  • immuno-inflammatory diseases
  • molecular pathways
  • translational research
  • molecular pathobiology
  • targeted therapy

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Published Papers (1 paper)

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Research

9 pages, 1270 KiB  
Article
Disturbed Complement Receptor Expression Pattern of B Cells Is Enhanced by Toll-like Receptor CD180 Ligation in Diffuse Cutaneous Systemic Sclerosis
by Szabina Erdő-Bonyár, Judit Rapp, Rovéna Subicz, Katalin Böröcz, Dávid Szinger, Kristóf Filipánits, Tünde Minier, Gábor Kumánovics, László Czirják, Tímea Berki and Diána Simon
Int. J. Mol. Sci. 2024, 25(17), 9230; https://doi.org/10.3390/ijms25179230 - 26 Aug 2024
Viewed by 1151
Abstract
Autoantibody production is a hallmark of systemic sclerosis (SSc) and the most extensively studied role of B cells in the pathogenesis of the disease. However, the potential involvement of innate immune molecules in B-cell dysfunction in SSc is less understood. B-cell activation is [...] Read more.
Autoantibody production is a hallmark of systemic sclerosis (SSc) and the most extensively studied role of B cells in the pathogenesis of the disease. However, the potential involvement of innate immune molecules in B-cell dysfunction in SSc is less understood. B-cell activation is an early event in the pathogenesis of SSc and is influenced by complement receptors (CRs) and Toll-like receptors (TLRs), shaping antibody responses. CR2 and CR1 modulate B-cell activation, and the roles of CR3 and CR4 are associated with autoimmune conditions. We investigated the expression of CRs in B cells from patients with the more severe form of the disease, diffuse cutaneous SSc (dcSSc), and the effect of TLR CD180 ligation on their expression. We found no significant difference in the basal expression of CD21 and CD11c in B cells between dcSSc and healthy controls (HCs). However, reduced basal CD11b expression in B cells in dcSSc compared to HCs, accompanied by a decrease in CD35 and an increase in CD11c expression following CD180 ligation may promote plasma cell formation and autoantibody production. Additionally, we searched for correlations between dcSSc-associated anti-DNA topoisomerase I (Scl-70) autoantibody, anti-citrate synthase (CS) natural autoantibody and complement component 3 (C3) levels and found a negative correlation between C3 and anti-CS autoantibody in dcSSc but not in HCs, supporting the hypothesis that natural autoantibodies could activate the complement system contributing to tissue injury in SSc. Full article
(This article belongs to the Special Issue Molecular Insights into Autoimmune Diseases)
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