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Cellular and Molecular Mechanisms of Autoimmune 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: 20 April 2025 | Viewed by 1333

Special Issue Editor


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Guest Editor

Special Issue Information

Dear Colleagues,

Autoimmune diseases are characterized by an impaired self-tolerance and by pathogenic antibodies against normal tissue proteins. These autoantibodies can directly damage their target tissues, or they can induce aberrant downstream effects, e.g., by stimulating signaling molecules. Various tissues such as the epidermis, thyroid, neuromuscular junction, myelinated nerves or the pancreas can be targets of such autoantibodies. Profound inflammation can be a result of autoimmunity, and the first line of treatment has traditionally been anti-inflammatory therapy with corticosteroids. However, more targeted therapies have started to emerge as our understanding of the molecular and cellular pathomechanisms is growing.

The purpose of this Special Issue is to highlight novel aspects of the cellular and molecular mechanisms of human autoimmune diseases. We encourage the submission of review articles and original research papers of any length. Our aim is to provide a comprehensive update on the pathomechanisms of autoimmune diseases at the cellular and molecular level.

Prof. Dr. Ritva Tikkanen
Guest Editor

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Keywords

  • autoimmune diseases
  • self-tolerance
  • immune cells
  • autoantibodies
  • autoantigens
  • pathomechanisms

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Published Papers (1 paper)

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Review

29 pages, 3375 KiB  
Review
Lymphocytes Change Their Phenotype and Function in Systemic Lupus Erythematosus and Lupus Nephritis
by Eleni Moysidou, Michalis Christodoulou, Georgios Lioulios, Stamatia Stai, Theodoros Karamitsos, Theodoros Dimitroulas, Asimina Fylaktou and Maria Stangou
Int. J. Mol. Sci. 2024, 25(20), 10905; https://doi.org/10.3390/ijms252010905 - 10 Oct 2024
Viewed by 1009
Abstract
Systemic lupus erythematosus (SLE) is a complex autoimmune disease, characterized by considerable changes in peripheral lymphocyte structure and function, that plays a critical role in commencing and reviving the inflammatory and immune signaling pathways. In healthy individuals, B lymphocytes have a major role [...] Read more.
Systemic lupus erythematosus (SLE) is a complex autoimmune disease, characterized by considerable changes in peripheral lymphocyte structure and function, that plays a critical role in commencing and reviving the inflammatory and immune signaling pathways. In healthy individuals, B lymphocytes have a major role in guiding and directing defense mechanisms against pathogens. Certain changes in B lymphocyte phenotype, including alterations in surface and endosomal receptors, occur in the presence of SLE and lead to dysregulation of peripheral B lymphocyte subpopulations. Functional changes are characterized by loss of self-tolerance, intra- and extrafollicular activation, and increased cytokine and autoantibody production. T lymphocytes seem to have a supporting, rather than a leading, role in the disease pathogenesis. Substantial aberrations in peripheral T lymphocyte subsets are evident, and include a reduction of cytotoxic, regulatory, and advanced differentiated subtypes, together with an increase of activated and autoreactive forms and abnormalities in follicular T cells. Up-regulated subpopulations, such as central and effector memory T cells, produce pre-inflammatory cytokines, activate B lymphocytes, and stimulate cell signaling pathways. This review explores the pivotal roles of B and T lymphocytes in the pathogenesis of SLE and Lupus Nephritis, emphasizing the multifaceted mechanisms and interactions and their phenotypic and functional dysregulations. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Autoimmune Disorders)
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