Question

Jenny Higgins, a 27-year-old female, develops achy joints, disrupted bowel activity and skin rashes over the course of 7 months. Although mild at first, the symptoms get worse over this time period, and while her GP did not initially suspect an autoimmune disease, Jenny is eventually diagnosed with Systemic Lupus Erythematosus (SLE) a classic systemic autoimmune disease. Answer the following sub-questions separately.

1) Name some common autoantibody responses present in patients with SLE? (1 mark)

2) Briefly describe how these autoantibodies contribute to symptoms of the disease.

3) Patients with SLE often have delayed clearance of apoptotic cells. Explain why this delay may result in an increased risk of autoreactivity to internal cellular components such as the nucleus.

4) If self-proteins or tissue components in the joints are not targeted directly in SLE, why do patients develop inflammation of joints?

5) Briefly describe a 2 stage (2 different drugs, and why you have chosen these) anti- inflammatory treatment regime designed to quickly bring inflammation under control, but moving to long term treatment more readily tolerated by the patient.

Answer 1

Answer

1. SLE is autoimmune disease.

some common antibody responce present in sle patients are antinuclear antibody , anti dsDNA ., anti SM , anti -Ro antibody , anti La antibody.

2. The antibodies in SLE patients are autoantibodies , this causes the immune system to target the body's own cell for destruction. some individual posses antiphospholipid antibodys which damages protien bound to phospholipids in the membrane of the cells . these affects orgons like lungs , kidney , heart ... these antibodies produces inflammation , vasculitis , immune complex deposition, and vasculopathy.

3 . SLE is chronic inflamatory disease , type 3 hypersensitivity .

impaired clerance of dying cell is potential pathway for development of this disease. early apoptotic cells express ' eat me 'signals of cell surface protiens such as phospatidylserine , that prompt immune cells to engulf them. apoptiotic cells also express' find me ' signal to attract macrophages and dendritic cells . when apoptotic cells are not removed correctly by phagocytes , they are captured instead by antigen presenting cells which leads to development of antinuclear antibody.

4. SLE patients develop temporary joint pain and tendonitis ,

here the protiens or tissues in joints are not directly attacked, but instead it is the type 3 hypersensitivity reaction, which leads to inflamation. this type of hypersensitivity reaction occures when accumulation of immune complexes (antigen antibody complexes ) that have not been adequately cleared by innate immune cells , give rise to inflamatory responce and attraction of leukocytes. so patient develop swelling , pain , warmth , redness over joints like finger , wrists , elbow , knee , toes.

5 . the drugs used in acute SLE patiennts are

nonsteroidal antiinflamatory drugs to reduce pain and inflamation

example - ibuprofen , naproxen

corticosteroids - this will decrease the process in body that makes inflamatory responce , it reduces activity of immune system by affecting function of white blood cells .

imunosuppresive medications like methotrexate , azathioprine. are used for long term controll of diseases.