Lupus erythematosus

Lupus erythematosus (also known as systemic lupus erythematosus or SLE) is an autoimmune disorder in which antibodies are created against the patient's own DNA. It is named for the Latin lupus, meaning "wolf," due to the butterfly-shaped rash that the disease classically creates on the cheek which medieval people believed to resemble a wolf bite.

Pathophysiology

Causes

The exact cause of the disease is unknown, and there is no consensus on whether it is a single condition or a group of related diseases. SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response, which is characterised by the body's production of antibodies against the nuclear components of its own cells. Some researchers have sought to find a connection between certain infectious agents (viruses and bacteria), but no pathogen can be consistently linked to the disease. Certain medications (such as some antidepressants) and environmental factors (such as exposure to sunlight) have been found to exacerbate symptoms.

Related Topics:
Inflammatory - Hypersensitivity - Virus - Bacteria - Antidepressant

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Research indicates that SLE may have a genetic link. People with SLE have an altered RUNX-1 binding site, which may be either cause or contributor (or both) to the condition. Altered binding sites for RUNX-1 have also been found in people with psoriasis and rheumatoid arthritis.

Related Topics:
Genetic - RUNX-1 - Psoriasis - Rheumatoid arthritis

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Abnormalities in apoptosis

• Apoptosis is increased in monocytes and keratinocytes
• Expression of Fas by B cells and T cells is increased
• There are correlations between the apoptotic rates of lymphocytes and disease activity

Tingible body macrophages (TBMs) are large phagocytic cells in the germinal centers of secondary lymph nodes. They express CD68 protein.

Related Topics:
Tingible body macrophage - Germinal center - Lymph nodes

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These cells normally engulf B cells which have undergone apoptosis after somatic hypermutation.

Related Topics:
B cells - Apoptosis - Somatic hypermutation

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In some patients with SLE, significantly fewer TBMs can be found, and these cells rarely contain material from apoptotic B cells. Also, uningested apoptotic nuclei can be found outside of TBMs. This material may present a threat to the tolerization of B cells and T cells.

Related Topics:
B cell - T cell

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Dendritic cells in the germinal center may endocytose such antigenic material and present it to T cells, activating them.

Related Topics:
Dendritic cell - T cell

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Also, apoptotic chromatin and nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells which may have randomly acquired self-specificity through somatic hypermutation.

Related Topics:
Follicular dendritic cell - B cell - Somatic hypermutation

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Complement pathway

SLE is associated with defects in lectins and the classical complement pathway.

Related Topics:
Lectin - Classical complement pathway

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