This month's Spotlight on... reviews autoimmune lymphoproliferative syndrome (ALPS) and its treatment. ALPS is an inherited disease caused by defects in lymphocyte apoptosis that cause nonmalignant proliferation of lymphocytes with autoimmune manifestations. Although there is yet no specific treatment for ALPS, therapies selectively targeting lymphocyte apoptosis may open a new avenue in the treatment of this rare disorder.
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INDOLENT CLONAL LYMPHOID DISORDERS.
Hum Pathol
January 2025
University Health Network and University of Toronto, Canada.
Indolent clonal lymphoid disorders are not recognized as lymphomas as they generally need no systemic treatment, and depending on the lesion, need only limited clinical follow-up. These lesions are usually incidentally diagnosed during the work up for other disease. The recognition of indolent clonal lymphoid disorders is important to avoid misdiagnosis as lymphoma and unnecessary treatment.
View Article and Find Full Text PDFIntroduction: Primary immunodeficiency diseases (PIDs), are a growing group of rarely seen diseases. Various clinical conditions like autoimmunity, lymphoproliferative/malignant diseases, chronic lung and gastrointestinal system diseases have been identified which accompanies PIDs besides recurrent infections. However, there is a lack of information about accompanying cardiovascular diseases.
View Article and Find Full Text PDFDistinct subtypes of post-transplant lymphoproliferative disorders: CHIP-like mutations in early lesions and substantial mutational differences between EBV-positive and EBV-negative diffuse large B-cell lymphomas.
Br J Haematol
January 2025
Pathology, Institute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Basel, Switzerland.
Post-transplant lymphoproliferative disorders (PTLD) and lymphomas in immunocompromised individuals represent significant clinical challenges, with a limited understanding of their pathogenesis. We investigated a PTLD cohort (n = 50) consisting of 'early lesions' (infectious mononucleosis-like PTLD, plasmacytic and follicular hyperplasias), polymorphic PTLD and post-transplant diffuse large B-cell lymphomas (PT-DLBCL). The study also included 15 DLBCL with autoimmune/immunocompromised backgrounds (IS-DLBCL) and 14 DLBCL, not otherwise specified (DLBCL, NOS), as control.
View Article and Find Full Text PDFAdvanced whole transcriptome sequencing and artificial intelligence/machine learning (AI/ML) in imiquimod-induced psoriasis-like inflammation of human keratinocytes.
Biomedicine (Taipei)
December 2024
Million-Person Precision Medicine Initiative, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.
Introduction: Although the HaCaT keratinocyte model has been used in previous research to study the effects of antipsoriatic agents, there is still a lack of comprehensive understanding of the mechanism of imiquimod (IMQ)-induced proliferation and signal transduction in psoriasis-like keratinocytes.
Objectives: This study aimed to investigate the molecular mechanisms and pathways associated with psoriasis-like inflammation caused by IMQ in human keratinocytes.
Materials And Methods: HaCaT cells were exposed to different concentrations of IMQ to induce inflammation similar to that observed in psoriasis.
Angioedema due to acquired C1-inhibitor deficiency without hematological condition: a multicenter French cohort study of 34 patients.
J Allergy Clin Immunol Pract
January 2025
Sorbonne Université, service de médecine interne, AP-HP, Hôpital Saint Antoine, F-75012 Paris, France. Electronic address:
Background: Angioedema (AE) due to acquired C1-inhibitor deficiency (AAE-C1-INH) is a rare disease associating recurrent edema of mucosa and skin. Several underlying diseases have been reported, mainly lymphoproliferative diseases and monoclonal gammopathy. However, 15 to 20% of patients never exhibit such a hematological condition.
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