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Lupus erythematosus


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Lupus erythematosus

  1. 1. LUPUS ERYTHEMATOSUS Done by : AbdulrahmanSulaiman Al-Otaiq
  2. 2. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Autoimmune disease affecting multiple organ systems Relapsing (flares) and remitting course Protean clinical manifestations Etiology is unknown Female to male ratio is 9:1 Age of onset 16 to 55 years (65%) < 16 years (20%) > 55 years (15%)
  3. 3. pathogenesis Genetic susceptibility  involvement of human leucocyte antigen (HLA) class II gene polymorphisms. presence of anti-small nuclear ribonuclear protein, anti-nuclear ribonuclear protein and anti-DNA antibodies. hormones Increase in estrogen lead to ↑B cell differentiation & ↓In vitro apoptosis of PBMCs &↓TNF production, This will leads to B cell hyperactivity and the production of pathogenic autoantibodies. Disturbances of the immune response Environmental antigens and self antigens are taken up by antigen presenting cells (APCs). process the antigens into peptides & present them to T cells through their surface HLA molecules.  The activated T cells in turn stimulate the B cells to produce pathogenic autoantibodies.
  4. 4. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) - PATHOGENESIS Defective regulation of apoptosis Accelerated rate of apoptosis in macrophages mediated (in part) by T cells T-cell mediated APC apoptosis Defective clearance of apoptotic cells Increased cell death with nuclear antigens exposed Nuclear antigens DS-DNA, Smith, Sjogren’s syndrome A (SSA) and B (SSB) Deposition of autoantibody-nuclear antigen complexes
  5. 5. Main Pathology The plasma cells are producing antibodies that are specific for self proteins, namely ds-DNA Overactive B-cells Suppressed regulatory function in T-cells Lack of T-cells Activation of the Complement system
  6. 6. Overactive B-cells Estrogen is a stimulator of B-cell activity Lupus is much more prevalent in females of ages 15-45 Height of Estrogen production IL-10, also a B-cell stimulator is in high concentration in lupus patient serum. High concentration linked to cell damage caused by inflammation
  7. 7. T-cell Malfunctions Fc region switch ζ εγ Leads to malfunction in signaling and decreased IL-2 production Increased levels of Ca2+ Leads to spontaneous apoptosis
  8. 8. T-cell Signal Transduction
  9. 9. Activation of Complement System Complement system is activated by the binding of antibodies to foreign debris. In this case its over activation RBCs lack CR1 receptor Decreasing the affective removal of complexes
  10. 10. IgG Pathogen IgG is the most “pathogenic” because it forms intermediate sized complexes that can get to the small places and block them.
  11. 11. DNA is the Main man DNA is the main antigen for which antibodies are formed. Extracellular DNA has an affinity for basement membrane where it is bound by autoantibodies. Classical thickening of the basement membrane
  12. 12. THANK YOU Reference : Burket's Oral Medicine, chapter 5