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Sjogren's syndrome: Everything you always wanted to know about genetic and epigenetic factors.
Autoimmun Rev
December 2024
Rheumatology, Department of Medicine, University of Perugia, Piazzale Giorgio Menghini, 1, 06129 Perugia, Italy.
Primary Sjögren's syndrome (pSS) is a chronic, systemic autoimmune disease characterized by a wide spectrum of glandular and extra-glandular features. Genetic and epigenetic factors play an important role in the disease susceptibility and phenotype. There are a multitude of genes that have been identified as implicated in the pathogenesis of pSS, both in HLA and extra-HLA regions with a strong contribution given by genes in interferon signalling pathways.
View Article and Find Full Text PDFSjögren's syndrome: one year in review 2023.
Clin Exp Rheumatol
December 2023
Rheumatology Unit, Department of Medicine and Surgery, University of Perugia, Italy.
Primary Sjögren's syndrome (pSS) is a systemic autoimmune disorder characterised by the T-cell-mediated hyperactivation of B-cells and cytokine production. The condition may evolve from an asymptomatic, indolent course, with glandular involvement, to extra-glandular systemic manifestations up to lymphoma development. On tissue level, the typical feature is the lymphocytic infiltration of the salivary gland by B-, T- and antigen presenting cells, as mirrored by the diagnostic cornerstone role of minor salivary gland (MSG) biopsy.
View Article and Find Full Text PDFIdentification of Tensin-3 as a MALT1 substrate that controls B cell adhesion and lymphoma dissemination.
Proc Natl Acad Sci U S A
December 2023
Department of Immunobiology, University of Lausanne, Epalinges CH-1066, Switzerland.
Article Synopsis
- MALT1 is a protein that helps activate immune cells and can also contribute to cancer by affecting how other proteins work in the cell.
- Researchers found that Tensin-3, a protein that helps cells stick together, is affected by MALT1 in human B cells, meaning it gets cut or "cleaved" by MALT1.
- In studies with mice and human cancer samples, they discovered that when Tensin-3 is cleaved by MALT1, it can reduce how well B cells stick together and help cancer spread to other parts of the body.
Human tumor viruses: induction of three-dimensional alterations in the host genome structure.
Front Microbiol
October 2023
Department of Oral Biology and Experimental Dental Research, Faculty of Dentistry, University of Szeged, Szeged, Hungary.
Certain viruses called tumor viruses or oncoviruses are capable to change the gene expression pattern of distinct human or animal cell types in tissue culture, resulting in uncontrolled proliferation as well as a change in the social behavior of the infected cells: the oncovirus-transformed, immortalized cells are capable to form malignant neoplasms in suitable animal models. At present, seven human viruses are categorized as causative agents of distinct human malignancies. The genomes of human tumor viruses, typically encode viral oncoproteins and non- translated viral RNAs that affect the gene expression pattern of their target cells or induce genetic and epigenetic alterations contributing to oncogenesis.
View Article and Find Full Text PDFImmune dysregulation as a leading principle for lymphoma development in diverse immunological backgrounds.
Immunol Lett
November 2023
Laboratory Medical Immunology, Department of Immunology, Erasmus Medical Center, Rotterdam, the Netherlands. Electronic address:
Lymphoma is a heterogeneous group of malignancies arising from lymphocytes, which poses a significant challenge in terms of diagnosis and treatment due to its diverse subtypes and underlying mechanisms. This review aims to explore the shared and distinct features of various forms of lymphoma predisposing conditions, with a focus on genetic, immunological and molecular aspects. While diseases such as autoimmune disorders, inborn errors of immunity and iatrogenic immunodeficiencies are biologically and immunologically distinct, each of these diseases results in profound immune dysregulation and a predisposition to lymphoma development.
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