Test 4 Study Guide Part 8

Question 1

Immune system exposed to antigen not normally in circulation:
- Two examples:

Answer 1

• 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

Question 2

inner eye proteins escape -> autoantibodies may form -> may destroy injured and uninjured eye

Answer 2

Sympathetic ophthalmia Antibodies against other antibodies:

Question 3

Thyroglobulin escapes from thyroid -> autoantibodies and autoreactive T lymphocytes form -> destroy thyroid gland

Answer 3

Hashimoto’s thyroiditis:

Question 4

Self-antigen combines with foreign antigen (or hapten) altering it:
- One example:

Answer 4

Drug-induced thrombocytopenia purpura:

due to: aspirin, penicillin, sulfonamides, antihistamines, digoxin, and other haptens

Question 5

Antibodies against other antibodies:

- One example:

Answer 5

Rheumatoid arthritis:
Abnormal production of IgM type -> attack Fc IgG type -> antigen antibody complexes causes inflammation -> inflammation of joints and systemic issues

Question 6

Antibodies produced against foreign antigens may cross-react with self-antigens:

Answer 6

Rheumatic fever:
Streptococcus pyogenes infects -> antibodies produced against it -> cross reactivity antigens in heart and kidney -> heart damage, glomerular capillaries damage (glomerulonephritis)

Question 7

Glomerulonephritis:

Answer 7

Damage to capillaries of glomeruli, can be caused by rheumatic fever.

Question 8

Self antigens may be presented with MHC-2 complexes to helper T lymphocytes:

• Why does this occur?
• Example:

Answer 8

• 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

Question 9

Graves disease

Answer 9

MHC-2 -> autoantibodies against TSH receptor protein in thyroid -> antibodies overstimulate thyroid receptors -> hyperthyroidism

Question 10

beta pancreatic islet cells produce MHC-2 -> they are destroyed -> goodbye insulin producing cells

Answer 10

Type 1 diabetes mellitus

Question 11

Inadequate activity of regulatory (suppressor) T lymphocytes:
- What factor causes T lymphocytes to become regulatory T cells?

Answer 11

• What factor causes T lymphocytes to become regulatory T cells?
  FOXP3

Question 12

FOXP3

Answer 12

factor causes T lymphocytes to become regulatory T cells

Question 13

Immune Complexes:

Answer 13

Antigen-antibody complexes which are not attached to the membrane.
- they promote inflammation

Question 14

Immune complexes:

• Normal disposal:
• Health hazards:

Answer 14

• 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

Question 15

Systemic autoimmune disease:

Answer 15

Multiple causes
One Cause:
Spreading of immune complexes systemically in high levels

Question 16

Hepatitis B:

- Autoimmune disease caused:

Answer 16

• Autoimmune disease caused:

Periarteritis

Question 17

Periarteritis:

Answer 17

Immune complexes are caught in the fenestrations of the capillaries and cause widespread inflammation
- Hepitatis B causes this

Question 18

Rheumatoid arthritis:
= Cause:
- Location:
- Immune complexes:

Answer 18

= 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

Question 19

Rheumatoid factors:

Answer 19

IgM antibodies that bind to the Fc Portion of IgG antibodies -> creating immune complexes

Question 20

Rheumatoid arthritis:

• Symmetric effect?
• Systemic symptoms?
• Systemic symptoms are due to?

Answer 20

• 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

Question 21

Lupus:

• Is also called:
• Population predominately affected:

Answer 21

• Is also called:
  Systemic Lupus Erythematosus
• Population predominately affected:
  Women in child bearing years

Question 22

Systemic Lupus Erythematosus (SLE):

• Systems damaged:
• Cause of damage:

Answer 22

• Systems damaged:
  kidney, joints, skin, CNS and others
• Cause:
  Antinuclear antibodies (IgG) against their own chromatin, snRNP, and others, forming antigen antibody complexes systemically

Question 23

How does exposure to self antigens promoting formation of antinuclear antibodies occur?

Answer 23

Apoptosis causes continual exposure to these.

People with SLE lose tolerance to these antigens (don’t know why)

Question 24

Systemic Lupus Erythematosus (SLE):

• Glomerulonephritis:
• What dictates if you get it?

Answer 24

- Glomerulonephritis:
Immune complexes caught in glomeruli when its filtrating
- What dictates if you get it?
Genetics
Environment (UV light, some infections)