As of June 10th 2020 about 7.2 million individuals have tested positive for, and more than 410,000 have died due to COVID-19. In this review we outline the pathophysiology that underpins the potential use of anti-rheumatic therapies for severe COVID-19 infection and summarize the current evidence regarding the risk and outcome of COVID-19 in patients with systemic autoimmune diseases. Thus far there is no convincing evidence that any disease-modifying anti-rheumatic drug (conventional synthetic, biologic or targeted synthetic) including hydroxychloroquine, may protect against severe COVID-19 infection; answers about their possible usefulness in the management of the cytokine storm associated with severe COVID-9 infection will only arise from ongoing randomized controlled trials. Evidence on COVID-19 risk and outcome in patients with systemic autoimmune diseases is extremely limited; thus, any conclusions would be unsafe and should be seen with great caution. At present, the risk and severity (hospitalization, intensive care unit admission and death) of COVID-19 infection in people with autoimmune diseases do not appear particularly dissimilar to the general population, with the possible exception of hospitalization in patients exposed to high glucocorticoid doses. At this stage it is impossible to draw any conclusions for differences in COVID-19 risk and outcome between different autoimmune diseases and between the various immunomodulatory therapies used for them. More research in the field is obviously required, including as a minimum careful and systematic epidemiology and appropriately controlled clinical trials.
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http://dx.doi.org/10.1007/s00296-020-04629-x | 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.
View Article and Find Full Text PDFLancet Rheumatol
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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