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Dear Colleagues,

We are pleased to kindly invite you to contribute with your research to the special Issue: Cellular and Molecular Biology in Autoimmune Disease.

As autoimmune disease remain a major medical concern and the mechanisms responsible for their pathogenesis are still incompletely understood, new insights in this field are needed. Various cellular, molecular, and physiological mechanisms have been suggested as potential triggers for the loss of self-tolerance, which make immune cells unable to distinguish among “self” and “non-self” antigens. Cellular mechanisms coupled with various mechanisms at the molecular level initiate dysregulated intercellular communication and are involved in the pathogenesis of autoimmune disease. Both innate and acquired immune system have been determined to be involved at the molecular level.

New data into genetic susceptibility suggest that environmental triggers could act via cellular pathways containing disease-associated polymorphisms. The full and deep understanding of these mechanisms will allow an adapted therapy. Recent treatments are expected to simultaneously and specifically target several pathways in autoimmunity. Due to the heterogeneity of autoimmune mechanisms, the knowledge in this area are expected to lead to a personalized molecular medicine approach in the field of autoimmune disease. Your data are expected to contribute to new insights in this unravelled field and you are very welcome to join us.

Prof. Dr. Cristina Belizna
Guest Editor

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Keywords

autoimmunity
autoimmune disease
cellular biology
molecular biology
cellular pathways
self-tolerance
molecular mechanisms
pathogenesis
therapy
personalized molecular medicine

Published Papers (1 paper)

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30 pages, 1784 KiB

Open AccessReview

Osteoimmunology: The Crosstalk between T Cells, B Cells, and Osteoclasts in Rheumatoid Arthritis

by Mei Yang and Lei Zhu

Int. J. Mol. Sci. 2024, 25(5), 2688; https://doi.org/10.3390/ijms25052688 - 26 Feb 2024

Viewed by 1023

Abstract

Rheumatoid arthritis (RA) is an ongoing inflammatory condition that affects the joints and can lead to severe damage to cartilage and bones, resulting in significant disability. This condition occurs when the immune system becomes overactive, causing osteoclasts, cells responsible for breaking down bone, to become more active than necessary, leading to bone breakdown. RA disrupts the equilibrium between osteoclasts and osteoblasts, resulting in serious complications such as localized bone erosion, weakened bones surrounding the joints, and even widespread osteoporosis. Antibodies against the receptor activator of nuclear factor-κB ligand (RANKL), a crucial stimulator of osteoclast differentiation, have shown great effectiveness both in laboratory settings and actual patient cases. Researchers are increasingly focusing on osteoclasts as significant contributors to bone erosion in RA. Given that RA involves an overactive immune system, T cells and B cells play a pivotal role by intensifying the immune response. The imbalance between Th17 cells and Treg cells, premature aging of T cells, and excessive production of antibodies by B cells not only exacerbate inflammation but also accelerate bone destruction. Understanding the connection between the immune system and osteoclasts is crucial for comprehending the impact of RA on bone health. By delving into the immune mechanisms that lead to joint damage, exploring the interactions between the immune system and osteoclasts, and investigating new biomarkers for RA, we can significantly improve early diagnosis, treatment, and prognosis of this condition. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Therapy in Autoimmune Disease)

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