BIOL 53700 Lecture Notes - Lecture 1: Peripheral Tolerance, Cd74, T Helper Cell

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harlequinzebra71

4 Mar 2018

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Biol 537 exam 2 study guide: every t cells initially start with the same genomic dna. I molecules begins by the process of cystoic pathogens being synthesized in the cytosol. Mhc class i molecules can only present cystolic pathogens to be killed by cytotoxic cd8. First, peptides are generated from the ubiquitinated proteins in the cytosol by the proteasome. Next, peptides from the cytosol are transported by tap into the er and further processed before binding to mhc i molecules. The mhc i molecules cannot leave the er until they bind a peptide. Partly folded mhc class i alpha chains bind to the calnexin until beta2-microglobulin binds. The mhc class i alpha:beta2m complex is then released from calnexin, binds a complex of chaperon proteins (calreticulin and. Cystolic proteins are degraded to peptide fragments by the proteasome and tap delivers the peptides to the er. A peptide then binds the mhc class i molecule and completes its folding.

Related Questions

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

1.How do some pathogens prevent complement activation or avoid the effects of activated complement?

A. some pathogens hijack the host's regulatory membrane proteins that inactivate C3b, preventing the triggering of the alternative activation pathway AND some pathogens produce C5a peptidase that causes destruction of phagoctyes recruited to the area of infection

B. some pathogens produce C5a peptidase that causes destruction of phagoctyes recruited to the area of infection

C. some pathogens produce C5a peptidase that destroys complement C5a, a chemoattractant that recruits phagocytes to the area of infection

D. Some pathogen hijack the host's regultory membrane proteins that inactivate C3b, preventing the triggering of the alternative activation pathway AND some pathogens produce C5a peptidase that destroys complement C5a, a chemoattractant that recruits phagocytes to the area of infection.

2. One of the most important jobs of dendritic cells is

A. production of complement proteins

B. activation of T cells by breakdown of whole antigens and presentation of antigenic epitopes on MHC molecules

C. stimulation of cytokine production by neutrophils

D. activation of B cells by combining epitopes and presentation of whole antigens on MHC molecules

E. production of IgD

3. Normal Microbiota

A. play no role in affecting pathogen growth

B. are the organisms that typically reside on and in your body

C. enhance infection by pathogens

D. are the organisms that typically reside on and in your body AND protect aganist infection by pathogens

E. protect against infection by pathogens.

4. why is the process of gene rearrangement used in creating antibodies and T-cell receptors (TCRs) so important?

A. the given choices are all reasons that generearrangement is critical in adaptive immunity

B. This is how our systems produce memory of previous exposures, a key trait in adaptive immune responses

C. without it, we would need a single gene for every antibody and TCR required to mount all the possible responses needed during our lives

D. interactions with antigens stimulate cells to initate these processes, building the best and strongest response possible to that antigen

E. this is the same DNA altering process that leads to cancer. Understanding it leads to better treatments for cancer.

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 53700 Lecture Notes - Lecture 1: Peripheral Tolerance, Cd74, T Helper Cell

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