BIOL 4570 Chapter Notes - Chapter 6: Cytotoxic T Cell, Antigen Presentation, T Cell

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27 Feb 2020

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Generation of alpha: beta t cell receptor ligands: antigen processing ~ generation of peptides from native proteins, antigen presentation ~ peptide display at cell surface by mhc molecule. 6. 1 antigen presentation functions both in arming effector t cells and in triggering their. Effector functions to attack pathogen infected cells: cytotoxic t cells ~ cd8 t cells; primarily responsible for pathogen surveillance and cytolysis of somatic cells; function is to kill cells they recognize. 6. 3 peptides from cytosol are transported by tap into er and further processed before. 6. 4 newly synthesized mhc class i molecules are retained in er until they bind peptide: mhc class i deficiency ~ immunodeficiency due to defects in tap1 and tap2 have few. Mhc class i molecules on their cell surfaces: folding and assembly of complete mhc class i molecule depends on association of mhc class i alpha chain first with beta 2 microglobulin and then with peptide.

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Immunology worksheet help?

In people infected with human cytomegalovirus, class I MHC andb2-microglobulin are produced, but very little mature class I MHCis found at the cell surface. Inhibition of which of the followingmolecules by human cytomegalovirus may account for thisphenomenon?

A.	TAP
B.	Ii
C.	TCR
D.	CLIP
E.	RAG

Your chances of having the same MHC haplotype as your siblingare:

A.	1:2.
B.	1:4.
C.	1:16.
D.	1:8.
E.	1:1.

Which of the following is the BEST example of self-MHCrestriction of T cells?

A.	A T-cell clone is deleted when it binds too tightly to selfMHC.
B.	A T-cell clone responds more vigorously to a self-peptide thana foreign peptide.
C.	A T-cell clone recognizes foreign MHC.
D.	A T-cell clone only recognizes foreign peptides when presentedby self MHC.
E.	All of the above

MHC molecules:

A.	are conserved between individuals.
B.	bind repeating patterns found on pathogens.
C.	are recognized by T cells.
D.	are membrane-bound molecules found exclusively on T cells.
E.	are secreted by T cells and bind and neutralize antigen in theserum.

Tasmanian devils are a largely inbred population with littlediversity in the MHC. Which of the following would be a likelyoutcome of this?

A.	They would compensate for low diversity in the MHC with highdiversity in the TCR.
B.	They would compensate for low diversity in the MHC with highdiversity in the BCR.
C.	They would rely only on innate immune responses.
D.	They would be at higher risk of infection.
E.	All of the above

How many different MHC classical class I proteins does eachnucleated cell in a human heterozygous at the MHC locusexpress?

A.	Six
B.	Two
C.	Three
D.	One
E.	None. Only APC express class I.

MHC polymorphisms tend to cluster:

A.	in the peptide-binding groove.
B.	in the transmembrane domain.
C.	in the coreceptor contact residues.
D.	in the framework region.
E.	All of the above

A mutation that renders the MHC class II molecule DMnonfunctional would likely lead to:

A.	cells with no class II MHC.
B.	a deficiency in CD8⁺ T cells.
C.	cells with class II MHC only bound with CLIP.
D.	cells with class II MHC bound with a variety ofself-antigens.
E.	cells with no DO.

The human MHC locus is one of the most polymorphic regions ofthe genome. What does this mean?

A.	This region is regulated by many different mechanisms.
B.	Sequence variability is low in this region.
C.	There are many introns in this region.
D.	There are many different alleles of these genes.
E.	It has the most different genes.

10.

Which of the following is an example ofcross-presentation?

A.	An exogenous peptide being presented on MHC class II
B.	A B-cell antigen being presented to a T cell
C.	An endogenous peptide being presented on MHC class I
D.	An endogenous peptide being presented on MHC class II
E.	An exogenous peptide being presented on MHC class I

magentacamel430

Question XV. The genes encoding MHC class I and classII molecules are highly polymorphic in human populations. SpecificMHC allotypes have been associated with increased susceptibility orresistance to certain viral infections. This influence of MHCmolecules on disease susceptibility can be best explained by thefact that [complete the sentence and assess each subsequentstatement (135-138) as either factually correct (= âtrueâ) orincorrect (= âfalseâ)]:

This question has confused me. The use of the word "best" seemsto imply there is one answer that is true and all others are false.Please answer this question in the context that 1. you could onlypick ONE answer as the BEST, which one you would pick and 2. if youcould answer more than one as true/best which ones would betrue

135. viral infection of DCs results in the presentation of viralpeptides by MHC molecules, which stimulates the activation of naiveT lymphocytes.
136. T cells become restricted to either MHC class I or MHC classII allotypes during their thymic development and this determineswhether they become polarized towards TH1 or TH2 responses,respectively.
137. different MHC allotypes differ in their ability to distinguishharmful compounds from harmless self antigens.
138. different MHC allotypes bind different peptides and,therefore, some allotypes can present peptides from certain virusesbetter than peptides from other viruses.

amethystcod591

Tasmanian devils (Sarcophilus harrisii), the worldâs largest carnivorous marsupials, are facing extinction. Not from hunting, or habitat loss, but from within; a transmissible cancerous derivative of Schwann cells, responsible for devil facial tumour disease (DFTD). First seen in 1996, the disease has spread widely though the population, and is now estimated to be present in 80% of the population. With the grim prognosis of ~100% mortality in 12-18 months, animals that once went through multiple breeding cycles are now lucky to reproduce once before death, resulting in a 70% decline in their population over the past decade. The cancer is transmitted by biting (a common ritual used by these animals to establish and maintain social position), with cancer cells from one animal (the biter) being implanted in the wound inflicted on the other animal. Equally common in both sexes, the disease itself is more prevalent in animals higher on the social scale, presumably reflecting higher levels of social interaction (biting). The cancer is usually first evident as facial tumors, from which metastasis to cervical lymph nodes occurs, often followed by dissemination to other organ systems. Cause of death is by organ failure or by malnutrition in those with facial tumors large enough to prevent feeding. Based on what we have covered regarding the Major Histocompatibility Complex, you would expect the passage of a cancer from one individual to another* to be a rare event (to see just how rare, read the accompanying popular press piece from the New York Times). Here are some things that you already know: *Yes, some viruses can cause cancer (example: Hepatitis B virus and liver cancer), and you can transmit a virus from one individual to another; but that is not the same thing as passing the cancer itself. v Almost all nucleated cells express high levels of class I MHC proteins on their surface. v Class I MHC proteins collect peptides produced from endogenous proteins and display them at the cell surface. v Different Class I MHC proteins bind and display different peptides. v Developing cytotoxic T-cells that recognize self-antigens are eliminated. v Mature cytotoxic T-cells conduct surveillance by scanning the peptides displayed by class I MHC proteins. v Mature cytotoxic T-cells that recognize an antigen on a cell will kill that cell (recall that cytotoxic T cell activity is important in rejection of tissue transplants).

Before the questions:
v Tasmanian Devils are not immunosuppressed.
v Tasmanian Devil cytotoxic T-cells are not broken, they can kill cells.
So neither of those should be part of your answers.
This is an ongoing research topic with large gaps in our knowledge; we really donât fully understand how this works
and so there is no âcorrectâ answer. Your job is to provide a logical argument, with some research and details to
support your contention. Note that in questions 1 & 2 class I MHC should be part of your answer, but not in
question 3.

Questions:
1.) Acquiring DFTD is basically like receiving a transplant that is not rejected. How can that be? Suggest a possible
way this could occur. Be sure to explain why you think this would work, and then explain how you would test
that model to determine if it were correct. (10 point question).
2.) Canine Transmissible Venereal Tumor (CTVT) is the other know transmissible cancer in mammals. Unlike
DFTD, CTVT does not usually result in death. Do a little research on this disease and summarize how it is
different from DFTD. Provide an explanation as to why one is lethal and the other is generally not. (10 point
question).
3.) Recently, researchers at Washington State University determined that some Tasmanian devils had developed
resistance to this cancer. By scanning partial genome sequences of resistant and susceptible animals (a
complete devil genome has yet to be assembled) they identified a set of genes where mutations appeared to
enhance resistance. Speculate as to the function of the proteins these genes encode, and explain why that
might provide for resistance (note: they were NOT MHC genes).

Mainly need guidance/ideas for #1's 1 and 3!

BIOL 4570 Chapter Notes - Chapter 6: Cytotoxic T Cell, Antigen Presentation, T Cell

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