Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare autosomal recessive autoimmune disease, affecting many endocrine tissues. APECED is associated to the lack of function of a single gene called AutoImmune REgulator (AIRE). Aire knockout mice develop various autoimmune disorders affecting different organs, indicating that Aire is a key gene in the control of organ-specific autoimmune diseases. AIRE is mainly expressed by medullary thymic epithelial cells (mTECs), and its absence results in the loss of tolerance against tissue restricted antigens (TRAs). Aire induces the transcription of genes encoding for TRAs in mTECs. In this report, the analysis of AIRE's effect on the cellular proteome was approached by the combination of two quantitative proteomics techniques, 2D-DIGE and ICPL, using an AIRE-transfected and nontransfected epithelial cell line. The results showed increased levels of several chaperones, (HSC70, HSP27 and tubulin-specific chaperone A) in AIRE-expressing cells, while various cytoskeleton interacting proteins, that is, transgelin, caldesmon, tropomyosin alpha-1 chain, myosin regulatory light polypeptide 9, and myosin-9, were decreased. Furthermore, some apoptosis-related proteins were differentially expressed. Data were confirmed by Western blot and flow cytometry analysis. Apoptosis assays with annexin V and etoposide demonstrated that AIRE-positive cells suffer more spontaneous apoptosis and are less resistant to apoptosis induction.
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http://dx.doi.org/10.1021/pr100044d | DOI Listing |
Tissue-resident memory T (T) cells are crucial components of the immune system that provide rapid, localized responses to recurrent pathogens at mucosal and epithelial barriers. Unlike circulating memory T cells, T cells are located within peripheral tissues, and they play vital roles in antiviral, antibacterial, and antitumor immunity. Their unique retention and activation mechanisms, including interactions with local epithelial cells and the expression of adhesion molecules, enable their persistence and immediate functionality in diverse tissues.
View Article and Find Full Text PDFBiochem Biophys Rep
March 2025
Changchun Medical College, 6177, Jilin Street, Changchun, 130031, China.
The Transforming Growth Factor-beta (TGF-β) signaling pathway, with SMAD4 as its central mediator, plays a pivotal role in regulating cellular functions, including growth, differentiation, apoptosis, and immune responses. While extensive research has elucidated SMAD4's role in tumorigenesis, its functions within immune cells remain underexplored. This review synthesizes current knowledge on SMAD4's diverse roles in various immune cells such as T cells, B cells, dendritic cells, and macrophages, highlighting its impact on immune homeostasis and pathogen response.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Biochemistry and Molecular Biology, Life Science Faculty, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj, 8100, Bangladesh.
Multiple Sclerosis (MS) is an autoimmune and chronic disease in the brain and spinal cord. MS has inflammatory progression characterized by its hallmark inflammatory plaques. The histological and clinical characteristics of MS are shared by Experimental Autoimmune Encephalomyelitis (EAE).
View Article and Find Full Text PDFHeliyon
January 2025
Centro de Investigaciones Clínicas, Fundación Valle del Lili, Cali, Colombia.
Introduction: The area postrema, located on the floor of the fourth ventricle, regulates vomiting, fluid balance, osmoregulation, and immunomodulation. First documented in 1896, it has been a subject of scientific interest ever since. Area postrema syndrome (APS) is characterised by intractable nausea, vomiting, or hiccups, typically associated with neuromyelitis optica spectrum disorder (NMOSD).
View Article and Find Full Text PDFArthritis Rheumatol
January 2025
Division of Medicine, Department of Inflammation and Rare Diseases, UCL Centre for Rheumatology, University College London, London, NW3 2PF, UK.
Objective: Scleroderma is a life-threatening autoimmune disease characterized by inflammation, tissue remodelling, and fibrosis. This study aimed to investigate the expression and function of transglutaminase 2 (TGM2) in scleroderma skin and experimentally-induced dermal fibrosis to determine its potential role and therapeutic implications.
Methods: We performed immunohistochemistry on skin sections to assess TGM2 expression and localisation, and protein biochemistry of both SSc-derived and healthy control dermal fibroblasts to assess TGM2 expression, function and ECM deposition in the presence of a TGM2 and TGFβ neutralizing antibodies and a small molecule inhibitor of the TGFβRI kinase.
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