ANBI 470.3 Lecture Notes - Lecture 11: Thymus, Neutrophil, Antigen Presentation

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20 Jun 2018

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Adaptive/ Acquired Immunity

Major histocompatibility complex (MHC)

-MHC class 1

oTransmembrane protein complex on all cells

oAll protein produced in a cell are partially degraded and “presented” on the cell surface

in association (bound to) with MHC class 1

oViral, tumor surveillance

when a virus infects a cell its proteins are made in the cell and the virus proteins

will be placed on the surface of MHC class 1

messed up proteins like tumor is also presented on the surface

opresent on all cells of the body, every protein that is made inside a cell, some of it is

broken down, hydrolyzed into little peptides and presented on the surface of the cell in

associated with MHC class 1

-MHC class 2

oTransmembrane protein complex found only on specialized antigen presenting cells

(ACPs)

oProteins entering the cell vial phagocytosis and endocytosis are degraded and

“presented” on MHC class 2

oVial particles and bacteria

oonly present on cells that can take material from the environment and phagocytosis or

endocytosis them into the cell

Cell Types

B lymphocytes

oProduced and mature in bone marrow

oRecognize intact soluble antigen via transmembrane antibodies

oGeneration of Ab binding diversity

Random gene rearrangement Ab variable region

oB cell as new has antibodies present in its plasma membrane, every new B cell you make

has a unique antibody specificity to A molecule

oSo how do we get it to bind to essentially anything?

 random gene association

 any B cell comes out the gene is permanently reorganized by this

there are repeating segments of J, D,V all with different nucleotide sequences ( so code for different AA)

-44 Variable, 27 Diversity, 6 Joining

as a B cell matures one of each of the VDJ regions are brought together and joined to the constant

region

-this gives us unique DNA sequence that is randomly generated

-this is how each b cell can bind a different thing

recombination of 3 coding segments ( v, d, and j) of antibody variable region in each naïve B cell to

generate a diverse binding repertoire

-the "arms" of the antibodies are were we have gene rearrangement

light chain and higher chain◦

-there is a constant region that stays the same

Three clases of B cells:

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Document Summary

Mhc class 1: transmembrane protein complex on all cells, all protein produced in a cell are partially degraded and presented on the cell surface in association (bound to) with mhc class 1, viral, tumor surveillance. When a virus infects a cell its proteins are made in the cell and the virus proteins will be placed on the surface of mhc class 1. Mhc class 2: transmembrane protein complex found only on specialized antigen presenting cells (acps, proteins entering the cell vial phagocytosis and endocytosis are degraded and. Presented on mhc class 2: vial particles and bacteria, only present on cells that can take material from the environment and phagocytosis or endocytosis them into the cell. B lymphocytes: produced and mature in bone marrow, recognize intact soluble antigen via transmembrane antibodies, generation of ab binding diversity. Three clases of b cells: na ve: new b cell that has never seen an antigen/infection (its permanent gene rearrangement segment)

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

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!

HI HELP PLEASE I NEED ANSWERS TO ALL QUESTIONS PLEASE THANKS

1. during inflamation fluid will passively diffuse out of blod vessels into the nearby infected tissue. This implies all of the following EXCEPT

a.the osmolarity of the fluid surrounding infected tissues is higher than the plasma b the surrounding tissue will swell with excessive fluids c near by cappilaries have become more pearmeable d B-lymphocyte will differeniate to become plasma cell

2. which of the following best describe the qualities of most antigens?

a macromolecules that are foreign to the host b atomic elements that are not normally present in the human body c macromolecules tah tare produced by the host organism d atomic elements that are harmful or toxic

3. an adbantages to adaptive immunity is

a its memory cell that provide quicker larger and more efficient immune response upon second exposure to an antigen b its need for several cells to be activated over several days on first exposure c the ability for its individul cells to respond to many differnt pathogens d the use of antibodies that cause cells lysis and kill invading cells

4, an advantages of innate immunity is

a its a barrier taht prevent pathogens from entering into the body b the specifcity of its individual cell which specialize in the removal on one type of antigen c the numerous step in the activation of its cell that can prevent autoimmune disease d the use of the antibodies to cause cell lysis and kill invading cell

5. B- lymphocytes are categorized as part of the adaptive branch of the immune sys for all of the following reason but one Which of the following is NOT one part of reason B lyphocytes are considered part of the adaptive immunity?

a they produce memory cell when activated b their receptors will bind to only one antigen c they require costimulation from an activated T helper cell d thet are a first line of defense that can begin killing

6. Over lap in the innate and adaptive immune sys is seen in all of the following examples but one Which of the following examples does NOT illustrate the over lap of innate and adaptive immune resposes ??? adendritic cell presenting antigen on their MHC II proteins to T helper cells b macrophage becoming activated macrophages in response to cytokines realesed by T helper cells c natural killer cell causing of an abnoraml host cell lacking MHC proteins d Plasma cell that produce large amounts of IgE that will ultimetly allow mast cell to relase histamine

7. Which of the following examples below describe an autoimmune disease? a infection and death of T helper cells bya virus resulting in a loss of adaptive immunity b realse of bacterial endotoxins that block acetylcholine realse result is muscle paralysis c antibody binding to acetylcholine receptors of hte motor end palte resulting in muscle weakness.d uncontrolled cell division resulting in cell surface abnormalities recognized by natural killer cell.

8. Which of he following does NOT describe actions of interferon IFN? a virally infected cell can release interferon which attracts natural killer cell to attack and kill the IFN secreting cell b IFN binds to normal uninfected cell stimulating the activation of genes that produce anti viral proteins c IFN will attract macrophages to the secreting cell to be removed bt phagocytosis d IFN can penetrate the virla capsid and destroy the virus

ANBI 470.3 Lecture Notes - Lecture 11: Thymus, Neutrophil, Antigen Presentation

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