Final Exam Questions

Question 0

Trisha’s grandchild is 5 months old, what type of immune response do you expect the baby to have to H influenza?

Answer 0

Th2, because she’s under 9 months of age and is not yet producing Th1. Unless she’s breastfeeding…

Question 1

Trisha, an overbearing grandmother isn’t keen on vaccines. Her 5 month old grandchild gets H Influenza. What type of immune response do you want to generate to H influenza and why?

Answer 1

Th1 would be ideal - specific to bacteria and virus; decreases the chance for the infant to develop allergy response to the antigen

Question 2

Trisha’s daughter, mother of the child, volunteers to vaccinate herself instead of the baby, and then breastfed her baby. Is this a good strategy? Why or why not? Will the baby have immunological memory?

Answer 2

Yes. Mom would mount a Th1 response and pass IgA through the breast milk to the baby. Once she stops breast feeding, the baby will not be protected because the baby is not producing the Abs itself - thus, no immunological memory.

Question 3

Memory immune response differs from 1st time exposure, why?

Answer 3

at initial exposure, no adaptive immune response has been developed. It will take between 7 - 10 days to develop.
With secondary exposure, or immunological memory, Abs are already circulating and will mount a response much quicker (2 -3 days)

Question 4

H. Influenza vaccine is a conjugate vaccine. How does a conjugate differ from attenuated vaccines?

Answer 4

Conjugate: polysaccharide from the microbe + protein (to help it present in MHC IIs); the polysaccharaide (hapten) must be conjugated (to carrier) to mount an immune response. Weakest immune response.
Attenuated: weakened, but live, pathogen. It has been passed through other species so that it is no longer infectious to humans. Strongest immune response to this type of vaccine.

Question 5

45 y/o with osteoarthritis. Pain in knees and elbows. Has wheat hypersensitivity type IV. How does this differ from a wheat allergy?

Answer 5

Type 1 Hypersensitivity: allergies –> MHC releases IL4 –> produce a Th2 response –> IL-4 (up reg IgE specific for gluten); IL-5 (EOS growth) and IL-13 (mast cells and mucus production) –> IgE binds FceR on Mast/Eos for degranulation –> Histamine!
Type IV Hypersensitivity (T Cell mediated) actually drives a Th1 response (–> IFN gamma, IL 12, IFN alpha) instead which can lead to autoimmunity; gliadin = tissue transglutaminase and binds MHC II

Question 6

How does immunological response influence symptoms? Ex. why would a patient with a wheat hypersensitivity (type IV) have joint pain, rather than hives?

Answer 6

As the immunological responses differentiate, they produce “unique” different signals (cytokines) that bind to different receptors on different types of cells to cause a particular action.
For example: Type IV - T cell mediated response, secretes TNF alpha, which can induce bone reabsorption –> joint pain; alternatively, Type I - Th2 response induces B cell Ab class-switch to IgE, IgE binds FceR on EOS and Mast cells, causing degranulation –> histamine –> hives

Question 7

An individual with a wheat hypersensitivity is prone to infections in the winter. She is taking chinese herbal medicine that drives up her Th1 response. How would this affect joint pain?

Answer 7

This individual is already experiencing a Th1 response, so this will enhance the Th1 response, probably making the joint pain worse. Luckily, if the patient has any allergies, TNF alpha is cross-regulating IL4, suppressing the immunological response to allergens.

Question 8

An individual who is hypersensitive to wheat says that smoking marijuana makes their joint pain lessen. What are some reasons that you can think of for why this is happening?

Answer 8

1) Marijuana is decreasing the Th1 response
2) marijuana is suppressing the immune system and therefore lessening the immune responsee
3) marijuana might be stimulating a Th2 response (secretes IL4), which would downregulate Th1’s IFNgamma

Question 9

A 28 year old with MS is experiencing numbness in fingers and hands. You suspect that this was caused by an infection. How is autoimmunity related to infections?

Answer 9

The bystander effect: MO is eating bits of Myelin Basic Protein (MBP) and presenting it w/o the danger signal –> a bacteria or virus enters MO cytoplasm or via endocytosis (TLR), is also presented in MHC 1/2 and stimulates danger signal. The 2 signals allow for T cell binding, which can differentiate into either CD4 or CD8 T cells - these T cells can mistake the MBP as “foreign”, causing immune response to MBP rather than the infection.

Question 10

Why would you see relapsing MS, symptoms coming and going?

Answer 10

As a result of stimulation of an autoreactive CD4 T cell to MBP via MHC II pathway, B cells are stimulated to class switch Abs (IgG) and Abs will bind to the myelin sheath (MBPs) and cause MOs to eat the sheath. Oligodendricytes come in to re-myelinate. 
MBP was likely ALSO presenting in the MHC class I pathway, binding to CD8 T cell (which secretes IL12) making it autoreactive for MBP. CD8 killer T cell will kill any cell expressing MHC + MBP, often found on oligodendricytes. CD8 T cells deplete resources to remyelinate the axon.

Question 11

What 3 factors increase the risk of MS?

Answer 11

1) Distance from the equator (for the first 15 years of life) –> low Vit D
2) Being female, 7:1 ratio
3) Socioeconomic status… white people get it more

Question 12

Why would you give worms to an MS patient?

Answer 12

Worms drive a Th2 response –> secretes IL-4, which cross-regulates Th1’s IFN gamma, effectively shutting down the Th1 response which exacerbates MS. Th1/Th2 balance.

Question 13

Tanning beds. Melanoma on scalp. What are 2 ways to produce a danger signal for the tumor?

Answer 13

1. Coley Toxin - mash up bacteria and inject very near to the tumor site; this would elicit danger signal in MO that will also eat part of the tumor and incite immune reaction for both the bacteria and the tumor.
2. Infections
3. Gene therapy

Question 14

MAGE - tumor specific antigen for melanoma goes through MHC I. What cells, cytokines are involved? Explain immune response.

Answer 14

Tumor usually incited by virus –> integrates in DNA (upregs oncogene, supresses tumor suppressor gene), MAGE (TSA) is presented in tumor cell in MHC I without CD86 (not APC), tumor cell dies due to lack of blood supply via necrosis –> MO takes up dead cells, presents TSA secretes IL 12 –> Th1 response –> CD8 (hopefully) T cell secretes IL-12 and IFN gamma –> stimulates B cells, class switch to IgG and allows for opsonization and destruction.

Question 15

What are some ways that melanoma can evade the immune system?

Answer 15

1. Turn off CD86
2. produce TGF-beta to shut down the Th1 response
3. down regulate MHC expression

Question 16

Would immunotherapy from melanoma work to treat lung cancer?

Answer 16

Maybe - it depends on the type of immunotherapy:
Ex. Coley Toxins - probably
Ex2. TSA - no, they have different Ags.

Question 17

33 year old rockstar, experiencing tiredness, malaise - is HIV positive. You make him an anti-viral cocktail… what’s in it?

Answer 17

4 enzymes:
1 that blocks CCR5 so that it can’t bind the virus
1 that blocks reverse transcriptase (REV) so it can’t translate viral RNA into cDNA (viral)
1 that blocks integrase so cDNA cannot enter the nucleus and/or integrate with human DNA
1 that blocks protease from chopping up viral proteins into active peptides

Question 18

HIV + guy has allergies to wheat and soy. Explain why continually exposing himself to wheat and soy would be a bad idea for the disease progression. Include the viral life cycle.

Answer 18

gp 120 binds to CD4 and CXCR4 receptors to bring virus into T cell -> gp40 allows virus to fuse with membrane, sucking it into celll -> nucleocapsid core dissolves and releases contents into cytoplasm (RNA, REV, integrase and protease); RNA transcribed to cDNA, is integrated into human DNA (now called provirus) and waits (viral latency) until T cell is activated and begins transcribing its DNA (incl. viral cDNA), DNA is translated into proteins and chopped up and new viruses are made and released. When rockstar eats wheat/soy, he stimulates a CD4 response, inciting replication of this viral life cycle and CD8 T cells will begins destroying CD4 T cells –> immunocompromised.

Question 19

Rockstar quits band, 2 years later he tests negative for HIV. why?

Answer 19

Viral latency: if he doesn’t activate the CD4 T cells again, the virus remains dormant. Eventually there is cell turnover and CD4 T cells die –> less HIV virus. But the HIV virus can also live other places (ie follicular dendritic cells in lymph nodes), which could contribute to future infection.

Question 20

Is HIV an autoimmune disease? Why or why not?

Answer 20

No. The immune response is attacking the virus (which is foreign), not the cells in which it lives.