Question

1.One group of immune deficiency diseases is caused by an inability of CD8 effector T cells to kill virus-infected target cells, due to defects in cytotoxic vesicle exocytosis. Because of the inflammatory response that accompanies a normal virus infection, together with the prolongation of this response due to the inability to control the infection, patients with these disorders suffer from tissue damage caused by the infiltration of effector CD8 cells and activated macrophages into multiple organs. In addition, a subset of these patients also show increased susceptibility to extracellular and intracellular bacterial infections. This is because:

a. CD8 T cells in these patients are defective in producing IFN-g.

b. CD8 T cells are required to kill extracellular bacteria.

c. Some proteins required for cytotoxic vesicle exocytosis are required for phagosome–lysosome fusion.

d. Inflammatory cytokines in these patients are inducing macrophages to phagocytose red and white blood cells.

e. Persistent uncontrolled herpesvirus infections cause immunosuppressive effects on bacterial clearance mechanisms.

2.Unlike defects in antibodies or T cell functions, defects in complement components often lead to autoimmune-like symptoms, rather than to increased susceptibility to infections. This is because:

a. The complement pathway normally functions to clear immune complexes from the circulation.

b. The complement pathway is part of the innate, rather than the adaptive immune response.

c. Partial activation of the complement cascade promotes phagocytosis of host cells.

d. Complement components do not require antibodies to attack microbial pathogens.

e. Complement inhibitory proteins are up-regulated by complement activation.

3.Individuals that lack all T cells have the most severe form of immunodeficiency (SCID) and will not survive past their first birthday without a bone marrow transplant from a healthy donor. These individuals fail to make antibody responses to the normal childhood vaccines because:

a. SCID causes a defect in B-cell receptor signaling

b. Most antibody responses require T cell help for the B cells

c. Persistent infections in SCID infants disrupts hematopoiesis

d. They generally lack all B cells

e. SCID patients lack AID, so their B cells cannot undergo class switching

Answer 1

CD8 T cells in these patients are defective in producing IFN- This option is correct because '208 T cell kills the target cells by producing perforin and granzymes And also vieleases Some cytokine such as IA AKY TNF-a and TNF-B which provide host immune defense mechanism IfN-Y mediate antiviral state , it is Proinflammatory cytokine get that give indecation of inflammation, Also this activate macrophages that kill extracellular pathogen So increased susceptili bilety is due to lack of TEN-Y so option A is correct.