According to a study from World Health Organization's Global Burden of Disease, mental and neurological disorders have accounted for 13% of global diseases in recent years and are on the rise. Neuropsychiatric conditions or neuroinflammatory disorders are linked by the presence of an exaggerated immune response both peripherally and in the central nervous system (CNS). Cognitive dysfunction (CD) encompasses a complex group of diseases and has frequently been described in the field of autoimmune diseases, especially in multiple non-CNS-related autoimmune diseases. Recent studies have provided various hypotheses regarding the occurrence of cognitive impairment in autoimmune diseases, including that abnormally activated immune cells can disrupt the integrity of the blood-brain barrier (BBB) to trigger a central neuroinflammatory response. When the BBB is intact, autoantibodies and pro-inflammatory molecules in peripheral circulation can enter the brain to activate microglia, inducing CNS inflammation and CD. However, the mechanisms explaining the association between the immune system and neural function and their contribution to diseases are uncertain. In this review, we used clinical statistics to illustrate the correlation between CD and autoimmune diseases that do not directly affect the CNS, summarized the clinical features and mechanisms by which autoimmune diseases trigger cognitive impairment, and explored existing knowledge regarding the link between CD and autoimmune diseases from the perspective of the field of neuroimmunology.
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http://dx.doi.org/10.1016/j.fmre.2022.12.005 | DOI Listing |
J Dermatol Sci
December 2024
Department of Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan; Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Japan. Electronic address:
Background: Altered Fli1 expression is associated with various autoimmune diseases, yet its impact on B cells remains unexplored.
Objective: This study investigated the direct effects of Fli1 depletion on B cell populations, focusing on age-associated B cells (ABCs).
Methods: Splenocytes of Fli1 BcKO (Cd19-Cre; Fli1) and Cd19-Cre mice were analyzed flow cytometrically.
Adv Clin Chem
January 2025
University of Toronto Lupus Clinic, Centre for Prognosis Studies in Rheumatic Diseases, Toronto Western Hospital, Toronto, ON, Canada. Electronic address:
Lupus nephritis (LN) or renal involvement of systemic lupus erythematosus (SLE), is a common manifestation occurring in at least 50 % of SLE patients. LN remains a significant source of morbidity, often leading to progressive renal dysfunction and is a major cause of death in SLE. Despite these challenges, advances in the understanding of the pathogenesis and genetic underpinnings of LN have led to a commendable expansion in available treatments over the past decade.
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January 2025
Department of Rheumatology, Université de Bretagne Occidentale, CHU Brest, INSERM (U1227), LabEx IGO Brest, France.
Background: Moderate doses of glucocorticoids result in improvements in nearly all patients with polymyalgia rheumatica, but related adverse events are common in older individuals. We aimed to evaluate whether treatment with baricitinib (a Janus kinase 1/2 inhibitor) results in disease control without the use of oral glucocorticoids in people with recent-onset polymyalgia rheumatica.
Methods: We conducted a randomised, double-blind, placebo-controlled, parallel-group trial at six expert centres in France.
Mol Ther
January 2025
Leibniz Institute for Immunotherapy (LIT), Division of Genetic Immunotherapy, Regensburg, Germany. Electronic address:
A rapidly growing number of chimeric antigen receptors (CARs) is being translated into cell therapy for malignant and autoimmune diseases. While cancer cell-selective CAR targeting is undergoing continuous refinement, specific testing for overlooked recognition of healthy tissues is commonly not performed, which potentially results in underestimating of the risk of severe tissue damage upon CAR T cell application. Using the FcμR/IgM receptor/FAIM3/TOSO-specific CAR, designed to target chronic lymphocytic leukemia cells, we exemplarily outline a screen to uncover reactivities to healthy tissues and discuss the value of such pre-clinical testing to improve safety in CAR T cell application.
View Article and Find Full Text PDFImmunobiology
January 2025
Department of Internal Medicine / Allergy and Clinical Immunology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Electronic address:
Background: Chronic spontaneous urticaria (CSU) is a persistent skin condition with no known cause or trigger. The unpredictability of CSU attacks lowers patients' quality of life. NOD-like receptor pyrin domain containing 3 (NLRP3) gene dysregulation can result in numerous immunological and inflammatory diseases.
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