Immunology Week 4

Question 1

Common allergies in children

Answer 1

milk, egg, peanut, wheat, soy, fish, shellfish

Question 2

Common allergies in adults

Answer 2

peanut, nuts, shellfish, fish, fruits/veggies mild

Question 3

What are the two types of food allergies and what are their typical symptoms?

Answer 3

IgE Mediated (urticaria, anaphylaxis), and non-IgE mediated (isolated GI reactions)

Question 4

What goes wrong in the GI tract with allergy?

Answer 4

Food proteins usually stimulate a Treg response. In allergy, Th2 cells are generated directing IgE antibodies AND/OR T cells may produce cytokines causing eosinophilic reaction (IL5)

Question 5

What happens in an IgE mediated allergy?

Answer 5

IgE specific for the food cross links, signals transduced, preformed mediators released (e.g., histamine). Clinical reactions ensue quickly

Question 6

Oral Allergy Syndrome (pollen food syndrome)

Answer 6

Mouth itch usually with no Sx outside of mouth. Birch pollen usually associated with stone fruit allergy, ragweed with melon allergy.

Question 7

Examples of non-IgE mediated allergies

Answer 7

enterocolitis, enteropathy, gastroenteritis, celiac. Eosinophilic esophagitis and atopic dermatitis in between.

Question 8

Eosinophilic esophagitis

Answer 8

basically a rash of the esophagus. Furrows, rings, or white plaques on endoscopy

Question 9

Anti-IgE

Answer 9

Binds only to Fc region of antibody

Question 10

Desensitization vs. tolerance

Answer 10

tolerance long term and independent of other variables (basically cured).

Question 11

EPIT

Answer 11

epicutaneus immunotherapy. Epithelial langerhans cells may induce regulatory and or Th-1 like responses with chronic exposure

Question 12

What deficiencies lead to spontaneous tumors?

Answer 12

RAG-1 or RAG-2, perforin, IFNgamma, IL-12 or

B2-microglobulin

Question 13

TILs

Answer 13

tumor infiltrating lymphocytes. Most often CD3

Question 14

Do solid tumors express costimulatory molecules?

Answer 14

NO

Question 15

Tumor Associated Antigens (TAA)

Answer 15

germline sequences normally silent, re-expressed embryonic antigens (not usually expressed, little tolerance), over expressed normal differentiation antigens, oncogenic viral antigens

Question 16

Some non-mutated TAAs on human tumors?

Answer 16

cancer testis antigens, MUC1, Her2/neu, CEA, MART-1, tyrosinase, HPV, EBV, HBV and HCV

Question 17

Some mutated TAAs on human tumors?

Answer 17

p53, p21ras,

Question 18

Tumor cells are antigenic, so why don’t effector cells kill them?

Answer 18

peripheral tolerance (essentially autoimmunity), secretion of inhibitory cytokines (TGFbeta and IL10), tumor cells aren’t seen as different, Loss of MHC expression by tumors so can’t be recognized by T cells,

Question 19

What happens to anti-tumor immunity as tumors increase?

Answer 19

It decreases

Question 20

Passive immunotherapy

Answer 20

The infusion of antibodies or mature T cells to the patient to attack the tumor.
This type of therapy does not induce permanent change in the patient’s own immunity. NO MEMORY, short lived

Question 21

Active immunotherapy

Answer 21

Tumor vaccines that directly stimulate the patient’s own immune cells to make a response against the tumor. Maybe long lived

Question 22

ADCC

Answer 22

antibody dependent cellular cytotoxicity - tumor destruction induced through antibodies and NK cells or eosinophils

Question 23

What are other ways antibodies can inhibit growth of cancer cells?

Answer 23

block receptors, deliver immunotoxins, or block checkpoint inhibitors (Prevents CTLA-4 or PD-1 engagement from inhibiting T cells)

Question 24

CTLA-4

Answer 24

blocking it prevents down regulation of T cell proliferation, can’t bind B7

Question 25

What is 5-FU?

Answer 25

cancer therapy drug

Question 26

Why is RAG important?

Answer 26

For VDJ recombination.

Question 27

Why is TAP important?

Answer 27

In the absence of TAP, peptides cannot enter the ER, so they are not loaded onto MHC class I molecules, also protecting the tumor cells from destruction by CD8+ cells.

Question 28

How can carbohydrates be recognized as antigens?

Answer 28

By antibodies, not by T cells

Question 29

How does X-linked agammaglobulinemia occur?

Answer 29

It occurs as a result of Bruton’s Tyrosine Kinase (BTK) deficiency. Don’t produce antibodies

Question 30

How does Hyper IgM occur?

Answer 30

Hyper-IgM syndrome results from a CD40L deficiency, causing lack of class switching, memory and affinity maturation.

Question 31

How does SCID occur?

Answer 31

There are many causes of SCID, which is a result of blocks in the maturation of both B and T cells.

Question 32

What’s the most common immunoglobulin deficiency?

Answer 32

IgA