Systemic Lupus Erythematosus
Systemic Lupus Erythematosus - Related Videos
12:04
The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
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Cited by 38 •
2015
The transfer of bm12 lymphocytes into a C57BL/6 recipient is an established model of systemic lupus erythematosus. Here we describe how to initiate disease using this model and how to characterize T follicular helper cells, germinal center B cells and plasma cells by flow cytometry.
05:44
Skin Biopsy for Diagnosing Discoid Lupus Erythematosus
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Cited by 2 •
2025
Skin lesions are common and important features in many rheumatic diseases, and biopsy with pathological analysis plays a critical role in diagnosis. This article provides a detailed overview of the standardized skin biopsy procedure and, using discoid lupus erythematosus as an example, highlights the essential role of dermatopathology in diagnosing rheumatic diseases.
05:39
Dermoscopy Aids in the Diagnosis of Discoid Lupus Erythematosus
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2025
Herein, we present a protocol to demonstrate the utility of dermoscopy in rheumatic diseases. In addition, we described the dermoscopic manifestations of discoid lupus erythematosus skin lesions.
13:19
The Use of Chemostats in Microbial Systems Biology
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Cited by 67 •
2013
Cell growth rate is a regulated process and a primary determinant of cell physiology. Continuous culturing using chemostats enables extrinsic control of cell growth rate by nutrient limitation facilitating the study of molecular networks that control cell growth and how those networks evolve to optimize cell growth.
01:18
Second Order systems II
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2024
In an underdamped second-order system, where the damping ratio ζ is between 0 and 1, a unit-step input results in a transfer function that, when transformed using the inverse Laplace method, reveals the output response. The output exhibits a damped sinusoidal oscillation, and the difference between the input and output is termed the error signal. This error signal also demonstrates damped oscillatory behavior. Eventually, as the system reaches a steady state, the error diminishes to zero. If ζ...
FAQs
These factors can combine to disrupt normal immune regulation and weaken tolerance to the body’s own components. Genetic susceptibility may create an underlying risk, while environmental triggers can promote abnormal immune activity. The resulting loss of regulation helps explain why SLE develops through multiple contributing influences rather than a single cause.
Antibodies directed against nuclear material are important because they can participate in the formation of immune complexes. These complexes activate inflammation, linking abnormal antibody production to tissue injury. Their role gives researchers a mechanism for examining how immune responses against cellular components may contribute to damage across several organs.
Immune complexes formed from autoantibodies and their targets can activate inflammatory processes. Inflammation may then affect tissues in organs such as the kidneys, skin, joints, lungs, heart, blood, and nervous system. This mechanism helps account for the broad clinical impact of SLE and the possibility of different organ patterns among affected individuals.
The overview indicates that symptoms may fluctuate, reflecting changing inflammatory activity within a disease shaped by genetic, environmental, and immune-regulatory factors. This variability is scientifically important because a patient’s condition may not remain constant. Studying these changes can support disease monitoring and help researchers relate immune activity to organ involvement over time.
Biomarkers provide measurable information that can support diagnosis and disease monitoring. In SLE research, they are especially valuable because the disease can involve multiple organs and symptoms may change over time. Investigators study biomarkers to improve recognition of disease activity and to evaluate whether biological changes correspond with inflammation or potential tissue damage.
A central goal is to design targeted treatments that limit inflammation and prevent or reduce organ damage. Research also examines the immune mechanisms underlying loss of tolerance, including abnormal autoantibody production and immune-complex activity. Connecting these mechanisms with clinical outcomes may support more focused approaches to controlling SLE while addressing its multisystem effects.