Test 4 Study Guide Part 8 Flashcards
Immune system exposed to antigen not normally in circulation:
- Two examples:
- Two examples:
Hashimoto’s thyroiditis:
Thyroglobulin escapes from thyroid -> autoantibodies and autoreactive T lymphocytes form -> destroy thyroid gland
Sympathetic ophthalmia:
inner eye proteins escape -> autoantibodies may form -> may destroy injured and uninjured eye
inner eye proteins escape -> autoantibodies may form -> may destroy injured and uninjured eye
Sympathetic ophthalmia Antibodies against other antibodies:
Thyroglobulin escapes from thyroid -> autoantibodies and autoreactive T lymphocytes form -> destroy thyroid gland
Hashimoto’s thyroiditis:
Self-antigen combines with foreign antigen (or hapten) altering it:
- One example:
Drug-induced thrombocytopenia purpura:
due to: aspirin, penicillin, sulfonamides, antihistamines, digoxin, and other haptens
Antibodies against other antibodies:
- One example:
Rheumatoid arthritis:
Abnormal production of IgM type -> attack Fc IgG type -> antigen antibody complexes causes inflammation -> inflammation of joints and systemic issues
Antibodies produced against foreign antigens may cross-react with self-antigens:
Rheumatic fever:
Streptococcus pyogenes infects -> antibodies produced against it -> cross reactivity antigens in heart and kidney -> heart damage, glomerular capillaries damage (glomerulonephritis)
Glomerulonephritis:
Damage to capillaries of glomeruli, can be caused by rheumatic fever.
Self antigens may be presented with MHC-2 complexes to helper T lymphocytes:
- Why does this occur?
- Example:
- Why does this occur?
Cells which do not normally produce MHC-2 produce one and present a self antigen on it (may be due to viral infection) - Example:
Graves disease:
Thyroid cells produce MHC-2 -> autoantibodies against TSH receptor protein in thyroid -> antibodies overstimulate thyroid receptors -> hyperthyroidism
Type 1 diabetes mellitus:
beta pancreatic islet cells produce MHC-2 -> they are destroyed -> goodbye insulin producing cells
Graves disease
MHC-2 -> autoantibodies against TSH receptor protein in thyroid -> antibodies overstimulate thyroid receptors -> hyperthyroidism
beta pancreatic islet cells produce MHC-2 -> they are destroyed -> goodbye insulin producing cells
Type 1 diabetes mellitus
Inadequate activity of regulatory (suppressor) T lymphocytes:
- What factor causes T lymphocytes to become regulatory T cells?
- What factor causes T lymphocytes to become regulatory T cells?
FOXP3
FOXP3
factor causes T lymphocytes to become regulatory T cells
Immune Complexes:
Antigen-antibody complexes which are not attached to the membrane.
- they promote inflammation
Immune complexes:
- Normal disposal:
- Health hazards:
- Normal disposal:
Engulfed by phagocytic cells - Health hazards:
If produced in too high conc. they can outpace their phagocytosis and cause excessive inflammation and damage
Systemic autoimmune disease:
Multiple causes
One Cause:
Spreading of immune complexes systemically in high levels
Hepatitis B:
- Autoimmune disease caused:
- Autoimmune disease caused:
Periarteritis
Periarteritis:
Immune complexes are caught in the fenestrations of the capillaries and cause widespread inflammation
- Hepitatis B causes this
Rheumatoid arthritis:
= Cause:
- Location:
- Immune complexes:
= Cause:
Unknown, but T-cells do enter first, release cytokines, and cause proliferation of plasma cells
- Location:
Inflammation of synovial fluid of peripheral joints, causes damage to nearby joints
- Immune complexes:
IgM binds IgG -> immune complex -> extends inflammation attracts more immune cells
Rheumatoid factors:
IgM antibodies that bind to the Fc Portion of IgG antibodies -> creating immune complexes
Rheumatoid arthritis:
- Symmetric effect?
- Systemic symptoms?
- Systemic symptoms are due to?
- Symmetric effect?
It effects joints symmetrically (left and right wrist for example) - Systemic symptoms?
Fatigue, anorexia, weakness - Systemic symptoms are due to?
Tumor necrosis factor, IL-1, IL-6, and other pro-inflammatory cytokines in systemic circulation
Lupus:
- Is also called:
- Population predominately affected:
- Is also called:
Systemic Lupus Erythematosus - Population predominately affected:
Women in child bearing years
Systemic Lupus Erythematosus (SLE):
- Systems damaged:
- Cause of damage:
- Systems damaged:
kidney, joints, skin, CNS and others - Cause:
Antinuclear antibodies (IgG) against their own chromatin, snRNP, and others, forming antigen antibody complexes systemically
How does exposure to self antigens promoting formation of antinuclear antibodies occur?
Apoptosis causes continual exposure to these.
People with SLE lose tolerance to these antigens (don’t know why)
Systemic Lupus Erythematosus (SLE):
- Glomerulonephritis:
- What dictates if you get it?
- Glomerulonephritis: Immune complexes caught in glomeruli when its filtrating - What dictates if you get it? Genetics Environment (UV light, some infections)
