Podcast
Questions and Answers
Which of the following scenarios best illustrates the interplay between genetic predisposition and environmental factors in the pathogenesis of SLE?
Which of the following scenarios best illustrates the interplay between genetic predisposition and environmental factors in the pathogenesis of SLE?
- An individual with no family history of autoimmune disease develops SLE after prolonged exposure to secondhand smoke.
- A person with SLE develops a photosensitive rash after sun exposure, despite having no known genetic risk factors for the disease.
- A patient with SLE develops lupus nephritis due to a bacterial infection.
- A woman with a family history of SLE experiences her first lupus flare after starting a new medication unrelated to autoimmune disease. (correct)
In SLE, how does the impaired clearance of apoptotic cells contribute to the amplification of the autoimmune response?
In SLE, how does the impaired clearance of apoptotic cells contribute to the amplification of the autoimmune response?
- By increasing the availability of nuclear antigens, stimulating the production of antinuclear antibodies (ANAs). (correct)
- By promoting the differentiation of regulatory T cells, which suppress the activity of autoreactive lymphocytes.
- By enhancing the phagocytic activity of macrophages, resulting in the rapid removal of immune complexes.
- By preventing the presentation of autoantigens to T cells, leading to decreased T cell activation.
How do excessive neutrophil extracellular traps (NETs) contribute to the pathogenesis of SLE?
How do excessive neutrophil extracellular traps (NETs) contribute to the pathogenesis of SLE?
- They release self-DNA and histones, exacerbating inflammation and stimulating autoantibody production. (correct)
- They inhibit the activation of plasmacytoid dendritic cells, decreasing interferon production.
- They promote the clearance of immune complexes, reducing inflammation.
- They release interferon-alpha, suppressing the adaptive immune response.
Why is the diagnosis of SLE often delayed, even in patients presenting with classic symptoms?
Why is the diagnosis of SLE often delayed, even in patients presenting with classic symptoms?
A researcher is investigating the role of T cell subsets in SLE. Which of the following findings would most strongly suggest a contribution of T cell dysregulation to SLE pathogenesis?
A researcher is investigating the role of T cell subsets in SLE. Which of the following findings would most strongly suggest a contribution of T cell dysregulation to SLE pathogenesis?
Which of the following best describes the mechanism by which UV radiation can trigger or exacerbate SLE?
Which of the following best describes the mechanism by which UV radiation can trigger or exacerbate SLE?
In the context of SLE pathogenesis, what is the role of B lymphocyte stimulator (BLyS), also known as B cell activating factor (BAFF)?
In the context of SLE pathogenesis, what is the role of B lymphocyte stimulator (BLyS), also known as B cell activating factor (BAFF)?
What is the rationale behind using immunosuppressive drugs, such as mycophenolate mofetil or cyclophosphamide, in the treatment of severe SLE?
What is the rationale behind using immunosuppressive drugs, such as mycophenolate mofetil or cyclophosphamide, in the treatment of severe SLE?
How does the genetic predisposition to SLE affect the body's ability to handle apoptotic cells?
How does the genetic predisposition to SLE affect the body's ability to handle apoptotic cells?
Which of the following mechanisms primarily accounts for the increased prevalence of SLE in women compared to men?
Which of the following mechanisms primarily accounts for the increased prevalence of SLE in women compared to men?
Flashcards
Systemic Lupus Erythematosus (SLE)
Systemic Lupus Erythematosus (SLE)
SLE is a chronic autoimmune disease where the immune system attacks the body's own cells, tissues, and organs.
Impaired clearance of apoptotic cells
Impaired clearance of apoptotic cells
Occurs when dead or dying cells aren't cleared, leading to the release of cellular contents that trigger an immune response.
Formation of Immune Complexes in SLE
Formation of Immune Complexes in SLE
Antibodies attack the body's own tissues, forming complexes that deposit in organs, causing inflammation and damage.
Multisystem Involvement in SLE
Multisystem Involvement in SLE
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SLE Epidemiology
SLE Epidemiology
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Genetic Predisposition to SLE
Genetic Predisposition to SLE
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Environmental triggers for SLE
Environmental triggers for SLE
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Excessive Extracellular Neutrophil Traps (NETs)
Excessive Extracellular Neutrophil Traps (NETs)
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T Cell Dysfunction in SLE
T Cell Dysfunction in SLE
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Autoantigens in SLE
Autoantigens in SLE
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Study Notes
Overview of Systemic Lupus Erythematosus (SLE)
- Systemic lupus erythematosus (SLE) is a chronic autoimmune disease.
- In SLE the immune system attacks the body's cells, tissues, and organs.
- SLE is a quintessential autoimmune disease, complex, multi-organ involvement and with an unpredictable course.
- SLE is heterogenous, changing in severity and symptoms over time in individual patients.
Complexity of SLE
- Multifactorial development includes impaired clearance of apoptotic cells
- Includes upregulation of innate and adaptive immune responses causing inflammation
- Includes formation of immune complexes where antibodies attack the body's own tissues, depositing in organs.
- Includes complement activation, causing inflammation and tissue damage.
Organ and Tissue Involvement
- SLE can affect any organ system, including kidneys (lupus nephritis), skin, joints, heart, and lungs.
- Symptoms can fluctuate over time in individuals
Epidemiology
- Worldwide, SLE primarily affects women (90%) aged 15-44.
- More prevalent in African descent, American Indians, and Alaska Natives, with more severe forms.
- Estimated 322,000 cases in the U.S., disproportionately affecting African Americans.
Pathogenesis of SLE
- Key factors include genetic predisposition and environmental triggers,
- Also include immune and inflammatory stimuli, with dysregulated immune responses.
- Defective clearance of apoptotic cells and immune complexes activates innate and adaptive immune responses
- Genes such as HLA, BLK, and STAP are associated with SLE.
- Environmental triggers include UV radiation, infections like Epstein-Barr Virus, and smoking.
Mechanisms of Disease Development
- T cells become defective and overly activated, shifting towards Th17 cells and double-negative T cells.
- UV-exposed keratinocytes release autoantigens, triggering immune responses and butterfly rash.
- Immune complexes deposit in tissues, causing inflammation and damage.
Immune Response in SLE
- Nuclear antigens are targeted by autoantibodies, forming antinuclear antibodies (ANA).
- Immune complexes circulate and deposit in tissues, causing inflammation and organ damage.
- Complement proteins are activated, leading to tissue injury and inflammation.
- Type III hypersensitivity reaction triggers inflammatory response.
Environmental and Genetic Triggers
- Cigarette smoking contributes to SLE development and exacerbation.
- Infections can trigger immune responses in genetically predisposed individuals.
- Certain medications, like hydralazine and isoniazid, can induce drug-induced lupus.
- Estrogen contributes to higher incidence in women during reproductive years.
Clinical Presentation of Lupus
- Common symptoms include fever, fatigue, joint pain, and the butterfly-shaped rash.
- Diagnosis is often delayed due to its variable and unpredictable symptoms.
- Diagnostic criteria include presence of ANA and immune complex deposition.
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