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Systemic lupus erythematosus is an autoimmune disease in which the body's immune system attacks healthy cells. How exactly do B and T cells attack these cells they mistake for pathogens?

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The initial trigger for the disease is unknown and can be different from person to person. However, we do know that there can be environmental or infectious triggers that are further potentiated by genetic and hormonal factors.

The pathology of SLE is associated with the development of "auto-antibodies" or "anti-nuclear antibodies," so saying that B cells and T cells attack healthy cells is not exactly correct - More accurately they produce antibodies against proteins on healthy cells, which form immune complexes, activate complement and induce apoptosis. To produce auto-antibodies, events occur as follows:

  1. The trigger causes macrophages or antigen-presenting cells (APCs) to display self- or auto-antigens
  2. APCs recruit B cells to start producing antibodies against the antigen
  3. APCs activate T helper cells, which stimulate inflammation and perpetually activate the B cells to produce auto-antibodies

The following immune abnormalities are associated with SLE (particular focus on B cells and T cells)

  1. High levels of circulating B cells
  2. Decreased levels of T suppressor cells, which would otherwise regulate the immune system and auto-antibody production
  3. Abnormal B cell signalling and persistent activation of B cells (IL-6, IL-10)
  4. Prolonged life span of B cells, possibly due to poor immunoregulation (#2)

Reference: Schur PH, Hahn BH, Pisetsky DS, Ramirez Curtis M. Epidemiology and pathogenesis of systemic lupus erythematosus. Up to date. Topic last updated: Feb 5 2016. Subscription access only.

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