Epstein-Barr virus (EBV)-positive mucocutaneous ulceration commonly presents as a B-cell lymphoproliferative process with manifold aspects. There is scarce data on its oral manifestation in the scientific literature. We report the case of a 57-year-old male immunocompromised renal transplant patient who developed recurrent chronic and symptomatic mucosal ulceration facing the mandibular incisor teeth. Pathological examination with microscopic and immunohistochemistry studies revealed a B plasma cell infiltration as well as positive staining for EBV, leading to a diagnosis of EBV-positive mucocutaneous ulceration with B-cell lymphoproliferation after extensive workup. Treatment with rituximab was implemented and led to the healing of the lesion. This lesion develops in geriatric and immunodeficient patients and may require oncological therapies. While it is generally associated with an excellent prognosis, it may be indicative of underlying immunosuppression, and hence oral cavity specialists must be aware of this particular entity.
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http://dx.doi.org/10.7759/cureus.42262 | DOI Listing |
Cell Death Differ
January 2025
Laboratory for Experimental Leukemia and Lymphoma Research (ELLF), LMU University Hospital, Munich, Germany.
The cell death receptor FAS and its ligand (FASLG) play crucial roles in the selection of B cells during the germinal center (GC) reaction. Failure to eliminate potentially harmful B cells via FAS can lead to lymphoproliferation and the development of B cell malignancies. The classic form of follicular lymphoma (FL) is a prototypic GC-derived B cell malignancy, characterized by the t(14;18)(q32;q21)IGH::BCL2 translocation and overexpression of antiapoptotic BCL2.
View Article and Find Full Text PDFPathogens
December 2024
Immunology and Vaccines Laboratory, Facultad de Ciencias Naturales, Universidad Autónoma de Querétaro, Campus Aeropuerto, Carretera a Chichimequillas, Ejido Bolaños, Querétaro 76140, Mexico.
SARS-CoV-2 () is responsible for the disease identified by the World Health Organization (WHO) as COVID-19. We designed "CHIVAX 2.1", a multi-epitope vaccine, containing ten immunogenic peptides with conserved B-cell and T-cell epitopes in the receceptor binding domain (RBD) sequences of different SARS-CoV-2 variants of concern (VoCs).
View Article and Find Full Text PDFCurr Opin Nephrol Hypertens
January 2025
Control of the immune response B and lymphoproliferation, CNRS UMR 7276, INSERM UMR 1262, University of Limoges, Centre de référence de l'amylose AL et autres maladies par dépôts d'immunoglobuline monoclonale, Limoges, France; Service de néphrologie et Centre National de référence amylose AL et autres maladies à dépôts d'immunoglobulines monoclonales, Centre Hospitalier Universitaire, Université de Poitiers, Poitiers, France.
Immunity
January 2025
Institute of Experimental Hematology, School of Medicine, Technical University of Munich, 81675 Munich, Germany; Center for Translational Cancer Research (TranslaTUM), School of Medicine, Technical University of Munich, 81675 Munich, Germany; German Cancer Consortium (DKTK), 69120 Heidelberg, Germany; Max-Planck Institute of Biochemistry, 82152 Planegg, Germany. Electronic address:
B cell immunity carries the inherent risk of deviating into autoimmunity and malignancy, which are both strongly associated with genetic variants or alterations that increase immune signaling. Here, we investigated the interplay of autoimmunity and lymphoma risk factors centered around the archetypal negative immune regulator TNFAIP3/A20 in mice. Counterintuitively, B cells with moderately elevated sensitivity to stimulation caused fatal autoimmune pathology, while those with high sensitivity did not.
View Article and Find Full Text PDFJ Clin Immunol
December 2024
Pediatric Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, University of Bologna, Bologna, Italy.
Background: Activated Phosphoinositide 3-Kinase (PI3K) δ Syndrome (APDS), an inborn error of immunity due to upregulation of the PI3K pathway, leads to recurrent infections and immune dysregulation (lymphoproliferation and autoimmunity).
Methods: Clinical and genetic data of 28 APDS patients from 25 unrelated families were collected from fifteen Italian centers.
Results: Patients were genetically confirmed with APDS-1 (n = 20) or APDS-2 (n = 8), with pathogenic mutations in the PIK3CD or PIK3R1 genes.
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