BIO 126 Lecture Notes - Lecture 4: Monocyte, Thymus, Apoptosis

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blackchimpanzee965

19 Sep 2016

School

Drexel University

Department

Bioscience & Biotechnology

Course

BIO 126

Professor

Kevin Smith

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Document Summary

Multiple molecules are involved in the activation and action of cytotoxic t cells. A cytotoxic t cell is activated through interaction with antigen-presenting cells and signals from helper t cells. Once a cytotoxic t cell has been activated, it can recognize an infected cell presenting a specific antigen fragment on its surface. The t cell receptor (tcr) recognizes the class i mhc-antigen fragment complex, and the cd8 protein on the cytotoxic t cell binds to the mhc molecule. To kill the infected cell, the cytotoxic t cell secretes perforin and granzymes. Perforin perforates the cell by forming pores, allowing granzymes to enter the cell and break down proteins. This leads to apoptosis, or programmed cell death. Once a cytotoxic t cell has induced apoptosis in a cell, it moves on to attack other infected cells or cancer cells. Protects against pathogens (living foreign invader that can make you sick)

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.

Which of the following is a characteristic of the adaptive immune system?

a .It is a specific response against microbial antigen

b. It includes inflammation.

c. It activates the alternative complement pathway.

d. It includes defenses on the body surfaces.

2. C-reactive protein is an opsonin because it:

a. creates a channel in bacterial membranes

b. increases C3b binding to a microbe.

c. forms the pathogen-associated molecular patterns.

d. enhances phagocytosis.

3. The rapid increase in antibody production after repeated exposures to the same antigen is due to:

a. antibody-dependent cellular cytotoxicity.

b. higher levels of IgE

c. presence of memory cells.

d. clonal proliferation of NK cells

4. Cytotoxic T cells can kill cancer cells by:

a. inducing apoptosis with granzyme.b. release of membrane attack complex.

c. activate the production of complement C3b

d. phagocytosis of opsonized cells.

5. Which event is not required for the activation of helper T cells?

a. The presence of interleukin-1

b. Binding of CD8 receptors

c. Binding of matching non-antigenic proteins of the antigen-presenting cel

d. Presentation of an antigen bound to class II MHC

plumworm266

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

BIO 126 Lecture Notes - Lecture 4: Monocyte, Thymus, Apoptosis

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