Component of the collaboration café

Follow these guidelines when completing each component of the collaboration café. Contact your course faculty if you have questions.

During the past four weeks, you have examined conditions affecting the immune, hematologic, cardiovascular, pulmonary, and renal systems. Some conditions can affect all of these conditions, including autoimmune disorders like systemic lupus erythematosus (SLE) that cause inflammation in multiple body systems. Follow the steps below to analyze the effects of SLE on various body systems.

Step 1: Review your assigned body system from weeks 1-4. Your assignment is based on the first letter of your last name in the chart below.

Last NameBody System

A – F Immune System

G – K Hematologic System

L – P Cardiovascular System

Q – U Pulmonary System

V – Z Renal System

Step 2: Reflect on how SLE impacts your assigned body system.

Step 3: Answer the discussion prompts below with explanation and detail, providing complete references for all citations.

Step 4: Reply to a peer with a different assigned body system.

Include the following sections:

  1. Application of Course Knowledge: Answer all questions/criteria with explanations and detail.

Describe the specific pathophysiological processes in SLE that lead to the manifestations observed in your assigned body system. How does SLE affect your assigned body system?
Discuss the symptoms and clinical manifestations of SLE on your assigned body system. How do these symptoms impact the client’s function and quality of life? Can changes in your assigned body system affect or be affected by other body systems in clients with SLE?
Discuss the diagnostic tests used to diagnose SLE-related complications in your body system. What challenges are associated with diagnosing SLE if only looking at your assigned body system?
Explore the current treatments for managing SLE symptoms associated with your assigned body system. What are the goals of these treatments and how effective are they in mitigating the impact of SLE on the body?

  1. Engagement in Meaningful Dialogue: Engage peers by asking questions and offering new insights, applications, perspectives, information, or implications for practice:

Respond to at least one peer.
Respond to a second peer post.
Communicate using respectful, collegial language and terminology appropriate to advanced nursing practice.

  1. Professionalism in Communication: Communicate with minimal errors in English grammar, spelling, syntax, and punctuation. 
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Collaboration Café: Systemic Lupus Erythematosus and the Immune System

 

1. Application of Course Knowledge

Describe the specific pathophysiological processes in SLE that lead to the manifestations observed in your assigned body system. How does SLE affect your assigned body system?

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease characterized by a dysfunctional immune system that paradoxically targets the body’s own tissues. The fundamental pathophysiological process in SLE is a breakdown of self-tolerance, leading to the production of autoantibodies against nuclear and cytoplasmic components of cells. This process is complex and involves genetic predispositions, environmental triggers (e.g., UV light, certain infections, medications), and hormonal influences (e.g., estrogen) (D’Cruz et al., 2007).

Full Answer Section

 

 

 

 

 

Specifically within the immune system itself, SLE is profoundly affected and simultaneously perpetuates its own pathology through several key mechanisms:

  • Loss of Apoptotic Debris Clearance: In healthy individuals, apoptotic (programmed cell death) bodies are efficiently cleared by phagocytes. In SLE, there is often impaired clearance of these dying cells, leading to an accumulation of nuclear material (DNA, histones, ribonucleoproteins) that becomes accessible to the immune system.
  • Activation of Innate Immunity: The uncleared apoptotic debris and immune complexes (ICs) containing self-antigens activate innate immune cells, particularly plasmacytoid dendritic cells (pDCs). This activation leads to the excessive production of type I interferons (IFN-), a cytokine critical to the pathogenesis of SLE. IFN- contributes to the maturation of dendritic cells, activation of B cells, and differentiation of T cells, thereby fueling the adaptive immune response (Rönnblom & Pascual, 2008).
  • B-Cell Hyperactivity and Autoantibody Production: A hallmark of SLE is B-cell hyperactivity, characterized by polyclonal activation, impaired tolerance checkpoints, and a shift towards plasma cell differentiation. These activated B cells produce a vast array of autoantibodies, most notably anti-nuclear antibodies (ANAs), but also anti-dsDNA, anti-Sm, anti-Ro/SSA, and anti-La/SSB antibodies. These autoantibodies form immune complexes with self-antigens.
  • T-Cell Dysfunction: T lymphocytes, especially CD4+ helper T cells, play a critical role in supporting B-cell autoantibody production. In SLE, there are imbalances in T-cell subsets, aberrant signaling pathways, and resistance to apoptosis, contributing to the persistent autoimmune response. Regulatory T cells (Tregs), which normally suppress immune responses, are often dysfunctional or reduced in number in SLE, further exacerbating autoimmunity (Crispin & Tsokos, 2011).

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