Microbiology and Immunology 2500A/B Study Guide - Final Guide: T Helper Cell, Naive T Cell, Mhc Class I

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emeraldhorse370

10 Jan 2017

School

Western University

Department

Microbiology and Immunology

Course

Microbiology and Immunology 2500A/B

Professor

Dr.Summers

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T-Cell Immunity Study Notes

•Primary immune response generates effector T-Cells. Some remain as memory effector T

cells.

•TCR only binds protein antigens.

•TCR must be presented with antigenic epitope on a Major Histocompatibility Complex (MHC)

molecule (hydrophilic so cannot bind to MHC molecule).

•Epitope = a peptide derived from a protein antigen.

•Each T cell expresses a variable region speciﬁc for one unique peptide (= epitope).

•There are two classes of MHC molecules: MHC 1 and MHC 2.

•All nucleated cells have MHC class I molecules.

•Cytotoxic T cells bind MHC class 1 peptide.

•Helper T cells bind MHC class 2 peptides.

•Peptides are generated from proteins inside a cell - which is where they bind to a MHC

molecule. The whole complex is then transported to the outside of that cell for presentation

to a T-Cell.

Endogenous Peptides

•Endogenous peptides are derived from intracellular

pathogens.

•Pathogen must replicate in the cytoplasm of an

infected cell.

•Intracellular bacteria are bacteria that avoid

phagocytosis and replicate in the phagosome or

cytoplasm. When the bacteria replicate in the

cytoplasm, this triggers T cell immunity. When it

escapes from phagosome, it produces endogenous

peptides.

•When a pathogen is replicating in the cytoplasm,

going to produce endogenous peptides. All nuclear

cells have proteasome (protein destroying

apparatus) - protein enters proteasome and gets

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chopped up into small fragments so all peptides coming out

are different and these are the endogenous peptides. Then

will go bind to MHC class 1 molecule and then get

transported to surface of the infected cell.

•All of our nuclear cells can potentially be affected by viruses.

Exogenous Peptides

•Exogenous peptides are presented on MHC class 2

molecules.

•Only specialized antigen-presenting

cells (APC) - have MHC class 2

molecules:

•dendritic cell (mature),

•macrophage,

•B cell.

•Why no neutrophils?

•Neutrophils have an extremely

short lifespan. Don’t live long

enough for the exogenous

peptides to go into MHC class 2

molecules and be presented.

•After degradation of pathogen in

phagolysosome, left with exogenous

peptides.

Dendritic Cells

•Dendritic cell role and function depends

on maturity state.

•Immature dendritic cells have a role in innate immunity and they are considered phagocytes.

•Mature dendritic cells (ones that have encountered a pathogen) have a role in adaptive

immunity and they are considered antigen-presenting cells that present MHC peptides.

•Dendritic cell and macrophages initiate adaptive immunity :

B-Cells

•How do B cells work as APC?

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•B cells internalize extracellular pathogen or

soluble protein by receptor mediated

endocytosis. The endosome fuses with the

lysosome, releasing enzymes and exogenous

peptides are presented on mHC class 2 cells.

•The BCR is recycled instead of being destroyed

like in phagocytosis.

•In

summary, APCs present exogenous peptides

on MHC class 2 molecules to helper T cells.

•Red blood cells (and all other non-nuclear

cells) do not have MHC molecules.

•APC can present both MHC class one and

two molecules.

Generating Effector T-Cells

•Dendritic cells are the only APC that can

activate naive T cells and generate effector T

cells.

•Immature dendritic cells resident in

secondary lymphoid tissue. DC meet pathogens in the blood (spleen), the lymph (LN), &

mucosa (MALT).

•The DC becomes infected or phagocytosis pathogen. It then presents peptides to circulating

naive T cells.

•Dendritic cell resides close to high endothelial venue (HEV).

•Very strategically located in the area where naive T cells will enter in.

•Probability of infected cell meeting naive T cell is high because of this structure.

•Immature dendritic cells resident in peripheral cells.

•Some immature DC infected with an intracellular pathogen or that have phagocytosed an

extracellular pathogen leave the tissue and migrate via lymphatics to the lymph node. DC

matures during migration and becomes APC. It arrives in T cell area of lymph node to

present peptide to naive T cells.

•Macrophages do NOT leave the

tissue.

•Effector T cells are the only

ones that can go back and

enter into inﬂamed peripheral

tissues.

•Express speciﬁc receptor

called CCR7 (chemokine)

which allows them to do this.

•Naive T cells do not express

this.

•effector cytotoxic T cells (CTLs)

= kills cell by apoptosis - same

process as natural killer cells.

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Document Summary

T-cell immunity study notes: primary immune response generates effector t-cells. The whole complex is then transported to the outside of that cell for presentation to a t-cell. Endogenous peptides: endogenous peptides are derived from intracellular pathogens, pathogen must replicate in the cytoplasm of an infected cell, intracellular bacteria are bacteria that avoid phagocytosis and replicate in the phagosome or cytoplasm. When the bacteria replicate in the cytoplasm, this triggers t cell immunity. When it escapes from phagosome, it produces endogenous peptides: when a pathogen is replicating in the cytoplasm, going to produce endogenous peptides. All nuclear cells have proteasome (protein destroying apparatus) - protein enters proteasome and gets chopped up into small fragments so all peptides coming out are different and these are the endogenous peptides. Then will go bind to mhc class 1 molecule and then get transported to surface of the infected cell: all of our nuclear cells can potentially be affected by viruses.

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

Q.1 (a) Production of which of the following types of proteinsduring an innate immune response would directly lead to the lysisof a microbe?

- Membrane Attack Complex

- Perforin

- Immunoglobulin

- Interferon

Q 1. (b) Swelling due to bulk flow from the plasma into theinterstital fluid is the result of decreased protein permeabilityin the capillaries. (True or False?)

Q.1 (c) Both inflammation and fever result in an increase in thetemperature set point of the body. (True or False?)

Q.1 (d) Indicate which of the following statements describeClass I MHC molecules, describe Class II MHC molecules or decribeboth Class I MHC & Class II MHC molecules?

-This molecule is expressed on all nucleated cells.

- This molecule interacts with proteins expressed on the surfaceof Cytotoxic T cells.

- This molecule is expressed on the surface of Antigenpresenting cells.

- This molecule is important for activating helper T cells.

- This molecule is expressed on the surface of B cells

- This molecule binds to antigens that come from primarilyintracellular pathogens.

Q.1 (e) What type of B cell does not secrete many antibodiesduring a primary immune response, but is very important for asecondary immune response?

Q.1 (f)If an individual failed to develop any maturelymphocytes, they would have lessened innate responses to infectionand lessened adaptive responses to infection. (True or False?)

Q.1 (g) Which of the following statements about the late stagesof HIV infection/AIDS are true? Choose all of the correctanswers.

		A person in the late stages of AIDS is more susceptible toinfection with bacteria, fungi and viruses than a person in theasymptomatic stage of HIV infection.
		The number of CD4-expressing T cells in the blood is high duringthe late stages of HIV infection
		The number of Killer T cells in the blood can be high during thelate stages of HIV infection.
		Innate immune responses may be weakened during the late stagesof HIV infection because of the weakened adaptive responses duringthese stages.

sapphirehare275

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!

Microbiology and Immunology 2500A/B Study Guide - Final Guide: T Helper Cell, Naive T Cell, Mhc Class I

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