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Lupus disease activity state and Foxp3 gene polymorphism.

Egypt J Immunol

January 2025

Department of Medical Microbiology and Immunology, Faculty of Medicine, Zagazig University, Zagazig, Egypt.

The autoimmune disease systemic lupus erythematosus (SLE) is presented with many clinical symptoms. The transcription factor fork head box protein 3 (Foxp3) is expressed on regulatory T (T-reg) cells and essential for its development and function. Functional single-nucleotide polymorphisms (SNPs) in the Foxp3-3279 (rs3761548 C/A) gene influence SLE pathogenesis.

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Impact of Fli1 deletion on B cell populations: A focus on age-associated B cells and transcriptional dynamics.

J Dermatol Sci

December 2024

Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan; Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Japan. Electronic address:

Background: Altered Fli1 expression is associated with various autoimmune diseases, yet its impact on B cells remains unexplored.

Objective: This study investigated the direct effects of Fli1 depletion on B cell populations, focusing on age-associated B cells (ABCs).

Methods: Splenocytes of Fli1 BcKO (Cd19-Cre; Fli1) and Cd19-Cre mice were analyzed flow cytometrically.

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Background: Systemic Lupus Erythematosus (SLE) is a typical autoimmune disease characterized by a complex pathogenesis and a strong genetic predisposition. The study of inflammatory response in SLE monocytes is not very clear, and exploring the inflammatory factors of monocytes is beneficial to discover new diagnostic targets.

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Introduction: Multiple Sclerosis (MS) is a complex auto-inflammatory disease affecting the brain and spinal cord, which results in axonal de-myelination and symptoms including fatigue, pain, and difficulties with vision and mobility. The involvement of the immune system in the pathology of MS is well established, particularly the adaptive T cell response, and there has been a particular focus on the IL-17-producing subset of Th17 cells and their role in driving disease. However, the importance of innate immune cells has not been so well characterised.

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Vitiligo is an autoimmune disease that has been recognized, stigmatized, and treated for millennia. Recent translational research has revealed key mechanisms of disease, including cellular stress, innate immune activation, T cell-mediated elimination of melanocytes from the skin resulting in clinically apparent white spots, as well as stem cell regeneration that reverses established lesions. Many of these pathways have been targeted therapeutically, leading to the first FDA-approved medication to reverse the disease, with many more in clinical trials.

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