MICR 270 Lecture Notes - Lecture 3: Mhc Class Ii, Signal Transduction, Dendritic Cell

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orangeelk876

12 Apr 2018

School

Queen's University

Department

Microbiology and Immunology

Course

MICR 270

Professor

Dr. Koti

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Document Summary

Phases of the adaptive immune response: antigen recognition. After invasion, pamps are seen by apcs (ex. dendritic cells and macrophages) Apcs process and present antigens to na ve t-cells via surface mhc proteins in order to activate adaptive immunity cells. Display antigenic peptides on the surface of cells. Recognized by the tcr and co-receptors (cd4 and cd8) to initiate a response. T-cells cannot recognize pathogens themselves and require an intermediate to present them (apcs) Apcs internalize pathogens, by phagocytosis or receptor-mediated endocytosis and process them into peptides to be displayed on the mhc on the surface of the apc. Most efficient, express through mhc class ii, express costimulatory signals. Antigens must be processed to form an effective mhc. Recognized by prrs and engulfed by apcs: proteolytic processing. Antigens inside endosome are broken down into fragments: formation of mhc-antigen complex. Vesicle containing fragments fuses with vesicles containing mhc molecule: cell surface expression.

Related Questions

Below is a paragraph describing HIV infection as they relate to the progress of infection. Please help choose the correct answer in each parentheses.

HIV initially infects (CD4+, or CD8+, or B) cells. These are helper T cells that activate (CD4+ or ,CD8+ or, B) cytotoxic T cells and (CD4+, or CD8+, or B) cells which produce antibodies. If HIV kills (CD4+, or CD8+) T cells then they cannot to do their job of activating these cells thus causing HIV infected people to be immunocompromised. Sometimes HIV infected people enter a latency period where the virus is inactive. This latency period can last for several years. During latency HIV (DNA, or RNA) becomes integrated into the (CD4+ or CD8+, or B) host cells genome and stops producing viral HIV RNA and new HIV virions. However, for some unknown reason, HIV comes out of dormancy and the viral (RNA, or DNA ) that was integrated in the (CD4+ , or CD8+,) T cell genome begins to transcribe more viral (DNA , or RNA) to make more viral (DNA, or RNA) using the host cells machinery. The viral (DNA, or RNA) then gets translated by host cell ribosomes to make viral proteins that eventually become packaged into new HIV virions. Consequently, after the latency period HIV becomes activated in the host cell. These cells present HIV antigen on their cell surface and alert (CD8+ or CD4+ or B) cells to kill them. As they are killed the infected (CD4+, or CD8+, or B) cells release the HIV virions into the blood stream to infect other (CD4+ or CD8+) cells such as macrophages and dendritic cells. This explains why after latency we see (CD4+, or CD8+) T cells continue to decrease while at the same time viral (DNA, or RNA) levels increase.

Based on your answers to the fill in paragraph, which statement is true?

A. Once active in CD8+ T cells, HIV can now replicate with impunity and infect other cells which explains the increase in HIV RNA after latency.

B. The increase in active HIV after latency accounts for why HIV can remain dormant for years after the initial infection.

C. CD4+ levels stabilize after the latency period and explain why there is little increase in HIV RNA levels.

D. Opportunist infections can occur after HIV latency because there are very few helper T cells to left to activate cytotoxic T cells and B cells to mount an immune response.

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.

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MICR 270 Lecture Notes - Lecture 3: Mhc Class Ii, Signal Transduction, Dendritic Cell

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