Type II Immunopathology and Regulation

Question 1

Type I immunopathology

Answer 1

Symptoms due to IgE antibody. Seen alongside Th2 mediated events

Question 2

Type II immunopathology

Answer 2

pathology due to IgM, IgG or IgA causing hard to self (autoantibodies.) Includes Type V, which stimulates rather than damages cells

Question 3

Type III immunopathology

Answer 3

Formation of immune complexes which get trapped in basement membranes of blood vessels and activate complement, leading to vasculitic inflammation.

When chronic, T-cell mediated responses become extremely important.

Question 4

Type IV immunopathology

Answer 4

Normal or abnormal T-cell responses causing pathology

Question 5

Chronic Frustrated Immune Response

Answer 5

body uses adaptive immune response against an antigen it can never get rid of!

Such as! Gut flora in Crohns, skin flora in psoriasis and gluten in Celiacs!

Question 6

How does complement mediated damage occur in Type II immunopathology? (3 methods)

Answer 6

1. ) Lysis - such as in autoimmune hemolytic anemia
2. ) Phagocytosis - autoimmune thrombocytopenia purpura
3. ) ROS/lysozymes - Myesthenia gravis/Goodpastures

Question 7

How does stimulatory hypersensitivity act in hyperthoidism?

Answer 7

Long acting thyroid stimulator

IgG antibody to TSH receptor, mimics TSH and causes cell to secrete thyroid hormone (Graves disease/hyperthydoism!)

Question 8

Myesthenia gravis

Answer 8

progressive muscle weakness b/c patients make antibody to the acetylcholine receptor. (antibody to the alpha subunit is what causes the most damage)

Thymic transcription factor Aira drives thymic expression of CHRNA (which is the gene for the alpha subunit…) -> but! its not expressed in the thymus! So T-cells reactive for the alpha subunit of the AchR isn’t taken out by negative selection!

Clinically: abnormal, hyperplastic thymus w/ germinal centers.

Question 9

How is myesthenia gravis treated?

Answer 9

Treated w/ thymectomy, immunosuppression, neostigmine-related drugs to increase effectiveness of AchR

Question 10

Rheumatic Heart Disease

Answer 10

occurs shortly after streptococcal infection, cross rxn between Group A Step M-protein antigen and laminin on endothelial lining _ heart valves.

Causes neutrophil mediated tissue destruction!

(Rheumatic fever is same disease only w/ systemic effects!)

Question 11

Dressler Syndrome

Answer 11

usually occurs after MI, direct immune response to pericardial/myocardial antigens (heart damage=proteins released that reg body doesn’t see=develop immune response!)

Manifests w/ [persistent cardiac pain, fever, malaise and pericadial effusion.

Question 12

Goodpasture Syndrome

Answer 12

formation of autoantibodies to lung and kidney basement membrane - antibody against Type IV collagen

Symptoms: persistent glomerulonephritis, pneumitis w/ pulmonary hemorrage

Question 13

Difference between immunoflourescence of sharp linear of Type II vs lumpy bumpy of Type III

Answer 13

One is linear one is lumpy bumpy lol

Question 14

Autoimmune Thrombocytopenic Purpura (ATP)

Answer 14

platelets are opsonized and and rapidly destroyed by the sleep

Treatment: remove sleep of suppress the immune system

Question 15

Autoimmune Hemolytic Anemia

Answer 15

follows a viral infection, may be associated with other autoimmune syndromes or cancer. Drugs like penicillin, methyldopa, chlorpromaze, quinidine can temporarily induce this state.

Rarely, you may have cold hemoglobinouria, where antibodies bind at 15 degrees C

Question 16

Systemic Lupus Erythematosus

Answer 16

has presence of rheumatoid factor = an IgM anti-IgG.

RA responds well to rituximab (monoclonal antibody against CD20 of B-cells)

RA linked to gene PAD14, antibodies to citrullinated peptides.

particularly important = antibodies against double stranded DNA? thats just no good.

Question 17

Hashimoto Thyroiditis

Answer 17

inflammatory disease of the thyroid, B and T cell immunity to thyroid antigens such as thyroglobulin. Thyroid filled w/ T-cells, so you have hypothyroidism!

Question 18

Name some mechanism by which type II Immunopathology may occur

Answer 18

1. ) Foreign+Self hybrid antigen - foreign antigens coupled to self. (foreign epitopes are present, B-cells signaled to be activated, but antibody is made to self)
2. ) Forbidden clone - clone may escape from clonal deletion, like in myesthenia gravis
3. ) Cross-Rxn - between foreign and self-antigen b/c they look alive! Woa!
4. ) Passive antibody - in child w/ hemolytic disease of the neborn, in patient w/ mismatched transfusion, or CHILD OF MOTHER W/ MYESTHENIA GRAVIS OF SLE
5. ) Innocent bystander - damage to tissue that is associated with intended pathogen
6. ) Release of sequestered antigen - like mumps and breakdown of blood/testis barrier - these antigens are usually hidden away, but once they’re out in the system, well! they are seen as foreign. :(

Question 19

Diagnosis of type II immunopathologies

Answer 19

Immunoflourescence!

1. ) Direct test: if you have a sample of pt’s tissue, add goat/rabbit antibody and tag w/ flourescence
2. ) Indirect test: can be done if you have pt’s serum. Normal kidney + patient’s serum w/ anti-GBM antibodies +label anti IgG!