GMS6540: IMMUNOSUPRESSANT DRUGS EXAM QUESTIONS
AND VERIFIED ANSWERS GRADED A++
purpose of immunosuppressive drugs
-prevention of organ transplant rejection
-treatment of autoimmune diseases = multiple sclerosis, lupus, rheumatoid arthritis,
crohn's disease, and type I diabetes
cellular basis for organ transplant rejection
1. antigen presenting cell (APC) activates T cells
2. T cells produce Interleukin 2 (IL2)
3. IL2 stimulates the proliferation of T cells and the production of additional cytokines
that stimulate the proliferation of multiple types of immune cells = T cells, B cells,
macrophages, etc.
4. activated immune cells attack transplanted organ (allograft)
molecular basis for organ transplant rejection
-T cell activated
-INCREASE in intracellular calcium within T cell
-calcium activates calcineurin = protein phosphatase
-dephosphorylates Nuclear Factor of Activated T cells (NFAT)
-NFAT once dephosphorylated goes to the nucleus
-activates expression of different genes = IL-2 mRNA
-IL-2 protein made and can act on other cells
-when IL-2 released it can bind to its own receptor = downstream activation of protein
, kinase mTOR
-mTOR important for proliferation of T cells
T/F: mTOR is important for the proliferation of T cells
True
Tacrolimus
-calcineurin inhibitor
-FK506/FKBP complex binds
-adverse effects = nephrotoxicity, hepatotoxicity, neurotoxicity
Cyclosporine
-calcineurin inhibitor
-intracellular receptor cyclophilin = complex binds
-adverse effects = nephrotoxicity, hepatotoxicity, neurotoxicity
prednisone
-inhibits cytokine production
-corticosteroid
-adverse effects = insomnia, hypomania, ulcers
drugs that are upstream of IL-2 production
-tacrolimus
-cyclosporine
-prednisone
daclizumab
-binds IL-2 receptor on activated T cells and neutralizes
sirolimus (rapamycin)
AND VERIFIED ANSWERS GRADED A++
purpose of immunosuppressive drugs
-prevention of organ transplant rejection
-treatment of autoimmune diseases = multiple sclerosis, lupus, rheumatoid arthritis,
crohn's disease, and type I diabetes
cellular basis for organ transplant rejection
1. antigen presenting cell (APC) activates T cells
2. T cells produce Interleukin 2 (IL2)
3. IL2 stimulates the proliferation of T cells and the production of additional cytokines
that stimulate the proliferation of multiple types of immune cells = T cells, B cells,
macrophages, etc.
4. activated immune cells attack transplanted organ (allograft)
molecular basis for organ transplant rejection
-T cell activated
-INCREASE in intracellular calcium within T cell
-calcium activates calcineurin = protein phosphatase
-dephosphorylates Nuclear Factor of Activated T cells (NFAT)
-NFAT once dephosphorylated goes to the nucleus
-activates expression of different genes = IL-2 mRNA
-IL-2 protein made and can act on other cells
-when IL-2 released it can bind to its own receptor = downstream activation of protein
, kinase mTOR
-mTOR important for proliferation of T cells
T/F: mTOR is important for the proliferation of T cells
True
Tacrolimus
-calcineurin inhibitor
-FK506/FKBP complex binds
-adverse effects = nephrotoxicity, hepatotoxicity, neurotoxicity
Cyclosporine
-calcineurin inhibitor
-intracellular receptor cyclophilin = complex binds
-adverse effects = nephrotoxicity, hepatotoxicity, neurotoxicity
prednisone
-inhibits cytokine production
-corticosteroid
-adverse effects = insomnia, hypomania, ulcers
drugs that are upstream of IL-2 production
-tacrolimus
-cyclosporine
-prednisone
daclizumab
-binds IL-2 receptor on activated T cells and neutralizes
sirolimus (rapamycin)
