Suppose you have two A-B-type exotoxins, A-B and A’-B’. A-B binds specifically to all

MHC-II cells and blocks vesicle trafficking. A’-B’ binds specifically to all MHC-I cells and

stops protein synthesis.

a. What would a hybrid toxin, A’-B, do to fibroblast (skin) cells? Provide your rationale.

b. What would a hybrid toxin, A-B’, do to fibroblasts? Provide your rationale.

c. What would a hybrid toxin, A’-B, do to macrophages? Provide your rationale.

d. What would a hybrid toxin, A-B’, do to macrophages? Provide your rationale

Immunology worksheet help?

1. Select which of the following are mechanisms used by pathogens to avoid host defenses and to successfully colonize the host.

A. Producing siderphores to obtain iron from the host for growth

B. producing adhesins for damaging host cells

C. Avoiding IgA proteases for avoiding secretory IgA

D. Avoiding secretory IgA by rapid turnover of pili

E. Producing toxic substances to suppress host responses

2. People considered obese have a different normal flora in the gastrointestinal tract compared to people who are considered lean.

A. true

B. false

3. Which of the following is NOT a mechanism used by pathogens for avoiding or surviving phagocytosis?

A. Killing macrophages and neutrophils

B. Colonizing the phagocyte

C. inhibiting opsonization

D. Inhibiting phagocte chemotaxis

E. these are all methods of avoiding or surviving phagocytosis

4.Which of the following immune responses is best suited to prevent a virus from infecting a cell?

A. complement cascade

B. inflammation

C. Virus-specific antibodies

D. Fever

E. phagocytic cells

5. Which of the following is NOT a method used by pathogens for penetrating skin or mucous membranes?

A. Injection of effector proteins that induce endocytosis

B. Exploiting antigen-sampling processes

C. these are all mechanisms for penetrating skin or mucous membranes

D. Exploiting an injury

E. Production of endotoxin

6. Antibodies, which are produced as part of the adaptive immune response, can sometimes be damaging rather than beneficial. People suffering from an autoimmune disease called antiphospholipid antibody syndrome (APS) make antibodies that bind to phospholipids. Some of the signs and symptoms affected individuals experience are blood clots, stroke, heart attack, and kidney damage. What is the likely cause of these symptoms?

A. the anti-phospholipid antibodies cuse immune complexes that lodge in the affected organs

B. The person fails to make protective antibodies

C. The anti-phospholipid antibodies weaken certain organs that contain fat

D. the person makes antibodies that bind inappropriately to bacterial capsules, preventing phagocytosis of these cells

E. Cell damage caused by binding of these antibodies initates inappropriate coagulation events which inferfere with blood flow in affected organs.

7. Only Gram-positive bacteria produce exotoxins

A. true

B. False

8. Which of the following members of the normal microbiota inhibit the growth of Candida albicans?

A. Lactobacilus species

B. Staphylococci species

C. E. coli

D. Neisseria species

E. Propionibacterium species

9. Would an antibody response against the B subunit of an A-B toxin protect against the effects of the toxin?

A. yes. if antibodies bind to the B protion, the toxin can no longer bind to target cells and will thus not affect those cells

B. No, even if antibodies bindto the B portion of the toxin, it is the A portion that actually causes damage to the cell

C. This question cannot be answer. The immune system does not mount a strong response against proteins, so this situation is unlikely to occur.

D. Yes, if antibodies bind to the B protein, that portion of the toxin does not become activated, and thus does not damage the host cell

E. No, even if antiibodies bind to the B portion of the toxin, the toxin is still taken into the host cell by phagocytosis, damaging that cell

10. Please select the correct definition of balanced pathogenicity.

A. A host-parasite relationship in which the parasite persists in the host, causing maximal harm. The pathogen becomes more virulent while the host becomes increasingly susceptible.

B. A mechanism that allows bacteria to transfer gene products directly into host cells, inducing changes such as altering the cell's cytoskeleton structure

C. A generated balance in the microbiome that may be caused by taking antimicrobial medication. it generally helps the host maintain optimal health

D. A situation in which an abnormally high number of T-helper cells are stimulated, causing a massive release of cytokines.

E. A host-parasite relationship in which the parasite persists in the host while causing minimal harm. The pathogen becomes less virulent while the host becomes less susceptible

11. Bacteria may survive phagocytosis by

A. preventing encounters with phagocytes AND preventing fusion of two pathogosomes

B. avoiding recognition and attachment of lymphocytes AND lysinf the phagosomes

C. preventing fusion of the lysosome with the phagosome AND mimicking host molecules

D. lysing the phagosome AND mimicking host molecules

E. preventing fusion of the lysosome with the phagosome AND lysing the phagosome

Given the scenario/situation, respond to all questions with complete sentences.

Scientists have been studying the effects of Starkagaren Disease, which is regulated by the stgn gene, in cultured normal and breast cancer cell lines. They have fused a yellow fluorescent probe to the end of the stgn gene to study the disease more closely. By adding a probe, it will create a hybrid protein that emits a yellow color under a blue laser. This hybrid protein is known as a fluorescent–tagged protein, meaning that the protein itself will function and fold normally but it will be tagged with a yellow fluorescent probe (YFP) at the end. This allows the scientists to follow the protein through the cell cycle. They find that the stgn protein normally binds to centromeres in normal cells. After looking at cells at various stages of the cell cycle, they find that compared to normal cells, the breast cancer cells that express the Starkagaren Disease display abnormal nuclei, some appear very large, some have tiny nuclei, and some cells do not have a nucleus at all.

a) Because the STGN protein binds to the centromere, the scientists can also study what other structure?

b) After looking the defects of the affected cells, where in the cell cycle would you guess the error occurs? What do you think happens?

c) The stgn gene appears to not be functioning, do you think the scientists are able to see the STGN protein at the centromeres? Why?

d) The scientists want to see what would happen if they could block the stgn gene from being made in normal cells or lung cancer cells, what is one way they could do this?