Multiple sclerosis (MS) is a complex autoimmune disorder that affects the central nervous system. Although the pathological mechanisms of MS have been extensively studied, its association with other autoimmune diseases, known as comorbidities, remains unclear. In this comprehensive review article, we aim to clarify the cellular and molecular relationship between MS and the incidence of organ-specific autoimmune comorbidities by summarizing former studies. We will explore the commonalities and possible differences between the immune response mechanisms in MS and other autoimmune diseases and provide an overview of the current understanding of the pathophysiological processes involved in the co-occurrence of MS and other organ-specific autoimmune comorbidities. Through this review, we aim to contribute to the development of effective therapeutic strategies that can improve the quality of life of MS patients with comorbidities.
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http://dx.doi.org/10.1007/s12035-024-04458-0 | DOI Listing |
Vestn Oftalmol
December 2024
AO Meditsina (Academician Roytberg's Clinic), Moscow, Russia.
Purpose: This study was conducted to identify the group at highest risk for autoimmune inflammation through a comparative analysis among patients with chronic post-traumatic uveitis (CPTU).
Material And Methods: The clinical group included 50 patients (aged 18 to 87 years, mean age 41±2.6 years) with CPTU resulting from penetrating injury, contusion, or intraocular surgery.
Arch Dermatol Res
December 2024
Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran.
Int J Biol Sci
December 2024
Department of Ophthalmology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, No.639, Zhizaoju Road, Huangpu District, Shanghai, China.
Thyroid eye disease (TED) is an organ-specific autoimmune disorder that significantly impacts patients' visual function, appearance, and well-being. Despite existing clinical evaluation methods, there remains a need for objective biomarkers to facilitate clinical management and pathogenesis investigation. Rapid advances in multi-omics technologies have enabled the discovery and development of more informative biomarkers for clinical use.
View Article and Find Full Text PDFNat Rev Rheumatol
January 2025
Translational Autoinflammatory Diseases Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Over the past two decades, the number of genetically defined autoinflammatory interferonopathies has steadily increased. Aicardi-Goutières syndrome and proteasome-associated autoinflammatory syndromes (PRAAS, also known as CANDLE) are caused by genetic defects that impair homeostatic intracellular nucleic acid and protein processing respectively. Research into these genetic defects revealed intracellular sensors that activate type I interferon production.
View Article and Find Full Text PDFType 1 diabetes (T1D) affects a genetically susceptible population that develops autoreactive T cells attacking insulin-producing pancreatic β cells. Increasingly, neoantigens are recognized as critical drivers of this autoimmune response. Here, we report a novel insulin neoepitope generated via post-translational cysteine-to-serine conversion (C>S) in human patients, which is also seen in the autoimmune-prone non-obese diabetic (NOD) mice.
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