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The association of the major histocompatibility complex (MHC) genes with autoimmune diseases together with the ectopic expression of class II molecules by epithelial cells of the target tissue gives to these molecules a central role in the pathogenesis of the disease, in its regulation and in the persistence of the immune response in situ. HLA-DR molecules expressed by thyroid follicular cells in thyroid autoimmune diseases are compact molecules stably associated with peptides. The nature of these peptides is of vital importance in the understanding of the disease, since these MHC-II-peptide complexes are going to be recognized by both effector and regulatory T cells in situ. In this chapter, we review the current state of the analysis of naturally processed peptides presented by MHC class II molecules in the context of autoimmunity and we discuss our data of natural HLA-DR ligands eluted from Graves' disease affected thyroid glands, from where autoantigen-derived peptides have been identified.
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http://dx.doi.org/10.1016/S0065-2776(08)00606-8 | DOI Listing |
Zhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha 410008.
Objectives: Patients with connective tissue diseases (CTD) have a high incidence of cardiac involvement, which often presents insidiously and can progress rapidly, making it one of the leading causes of death. Multiparametric cardiovascular magnetic resonance (CMR) provides a comprehensive quantitative evaluation of myocardial injury and is emerging as a valuable tool for detecting cardiac involvement in CTD. This study aims to investigate the correlations between CMR features and serological biomarkers in CTD patients, assess their potential clinical value, and further explore the impact of pre-CMR immunotherapy intensity on CMR-specific parameters, thereby evaluating the role of CMR in the early diagnosis of CTD-related cardiac involvement.
View Article and Find Full Text PDFParasite Immunol
September 2025
Department of Zoology, Panjab University, Chandigarh, India.
Leishmania parasite adeptly evades the host's immune defences by infiltrating macrophages, exploiting apoptotic processes for further dissemination. Among the host's strategies to counter parasitic propagation, the pivotal role of B-cells, specifically B regulatory (Breg) cells, emerges. Recent evidence from in vitro and in vivo studies has thrust Breg cells into the spotlight, attributed to their IL-10 secretion and antigen presentation.
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Department of Medical Biochemistry, Molecular Biology, and Immunology, School of Medicine, University of Seville, Spain; Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocio/CSIC/Universidad de Sevilla, Seville, 41013, Spain. Electronic address:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment, synaptic dysfunction, and neuronal loss. Neuroinflammation, driven by the activation of microglia and astrocytes, is a key contributor to AD pathology, amplifying oxidative stress and amyloid-β toxicity. Modulation of neuroinflammatory pathways thus represents a promising therapeutic strategy.
View Article and Find Full Text PDFAtherosclerosis
September 2025
Division of Biotherapeutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, the Netherlands. Electronic address:
Background And Aim: Atherosclerosis has an auto-immune component driven by self-reactive T and B cells. Identifying their antigenic drivers may lead to new diagnosis and treatment approaches. Here, we aim to identify immunogenic T cell epitopes derived from atherosclerosis-relevant proteins such as ApoB100 by studying the repertoire of peptides presented by HLA in human plaques.
View Article and Find Full Text PDFACS Nano
September 2025
School of Medicine, Nankai University, Tianjin 300071, China.
In situ articular cartilage (AC) regeneration is a meticulously coordinated process. Microfracture has been the most extensive clinical approach in AC repair, but it faces challenges such as matrix degradation, generation, and remodeling within a local inflammatory microenvironment. So far, it remains a challenge to establish a multistage regulatory framework for coordinating these cellular events, particularly the immune response and chondrocyte proliferation in microfracture-mediated AC repair microenvironments, which is crucial for promoting AC regeneration quality.
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