Introduction

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Systemic Lupus Erythematosus (SLE) is an autoimmune disorder commonly affecting the skin, musculoskeletal, renal, neurological, haematological, cardiovascular, and respiratory systems (1). It is characterized by widespread inflammation, autoantibody production, and immune complex deposition. While SLE affects multiple major organ systems in the body, lupus nephritis is the leading cause of death. Approximately two million people suffer from SLE with the majority of cases being women, with a female to male ratio of 9:1. African American, Hispanic, Asian, and Native American women are more likely to get SLE than Caucasian women (4).

 

The exact pathological mechanisms of SLE is unknown, and the cause of SLE is known to have multiple factors involved, including multiple genes, sex hormones, and environmental factors like sunlight, drugs and infections (5).  In SLE, immune homeostasis is impaired, and both T and B cells acquire abnormal characteristics in terms of activation, cytokine production, and proliferative potential (4). SLE can manifest with the appropriate genetic background, presence of immune triggers, and effective immune system activation. Disease-specific antibodies may circulate for up to five years before the first clinical signs of organ involvement in the disease (5).

 

Apoptosis is a programmed cell death and occurs during various biological processes.  Phagocytes then clear out the dead cells from tissues (2). A core hypothesis for SLE pathogenesis implicates poorly cleared or excessively produced apoptotic blebs as a constant source of partially degraded nucleosomes (5). Nuclear autoantigens targeted in SLE are clustered in blebs at the surface of apoptotic cells (2). Impaired clearance of dying cells in SLE may explain the accumulation of apoptotic cells in tissues, while secondary necrosis of these cells might contribute to the chronic inflammation that is seen in this disease (5). Apoptosis induced modified nuclear autoantigens are exposed to the immune system and recognized as non-self-antigens causing a danger signal. Plasmocytic dendritic cells respond to nucleic acid-containing immune complexes by producing type I interferon IFN-α. Ultimately, these processes result in an immunogenic response and the formation of autoantibodies to the modified nuclear autoantigens

(2).

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Symptoms

 

Symptoms of System Lupus Erythematosus, SLE, include:

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• Fatigue

• Skin Rashes

  • Butterfly rash across the face is common among SLE patients.

• Fevers

• Pain and Swelling of Joints

  • Similar to arthritis pain

 

These symptoms can occur all at once, spontaneously for a period of time, and go away suddenly. These periods are called flares and can happen years apart, some experiencing them more frequently than others. What triggers flares is unknown, but environmental factors and stress seem play a role.

 

Other symptoms SLE patients may experience include:

• sensitivity to the sun

• oral ulcers

• arthritis

• lung problems

  • plural effusions

• Heart problems

  • Myocarditis

• Kidney problems

  • Interstitial arthritis

• Seizures

• Psychosis

• Blood cell and immunological disorders