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14 Cards in this Set

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  • Back
Prednisone and Prednisolone (corticosteroids) MOA?
1. Leukocytopenia
2. Reduce size and lymphoid content of the lymph nodes and spleen
3. Interfere w/ fxn of macrophages/monocytes
4. Interfere's w/ fxn of helper T cells
5. Interferes w/ lymphokine synthesis
Explain the leukocytopenia.
1. Marked reduction in circulating T and B lymphocytes
-- cells redistrib to spleen, bone marrow
-- T cell content reduced more than B cell content
-- CD4 cells show greater decrease than do CD8 cells
-- Decreased circulating monocytes
-- Decreased circulating eosinophils and basophils
-- INCREASED circulating neutrophils due to release of mature cells from bone marrow and decreased movement from blood into vascular tissue
Explain how prednisone and prednisolone interfere w/ fxn of macrophages and monocytes?
They block expression of the genes for IL-1 (stims TH1 cells) and IL-6 (stims TH2, B cells, plasma cells)
Explain how prednisone and prednisolone interfere w/ fxn of helper T cells.
1. Block expression of genes for IL-2 and IL-4
2. Blocks expression of genes for TNFb and IFNg

1. No activation of TH1 and TH2 helper T cells
2. No activation of cytotoxic T cells
3. Prevents synthesis of TNF and IFNg by helper T cells
4. Reverses the increased expression of MHCII proteins and adhesion molecules by allograft cells
What are the net effects of corticosteroids (prednisone, prednisolone)?
1. prevent activation of T cells
2. prevent proliferation of T and B cells
3. suppress the production of antibodies by B cells
How do prednisone and prednisolone interfere with lymphokine synthesis?
**Block expression of the genes which code for IL-1, IL-2, IL-4, IL-6, IFNg, and TNF

1. inhibit expression of MHCII antigens by the allograft cells
2. prevent increased expression of adhesion molec by the vascular endothel cells of the allograft
3. inhib fxn monocytes/macrophages
4. inhib activation T helpers
5. inhib clonal expansion of T cells and B cells
6. inhib activation cytotoxic T cells
7. inhib Ab production
8. generalized inhib of cellular and humoral immunity
Cyclosporine MOA overview?
-- blocks T cell activation
-- prevents clonal expansion T cells, B cells
-- prevents action cytotoxic T cells
Cyclosporine MOA specifics?
1. Prevents transcription genes for IL-2, TNFb, and IFNg
2. Prevents transcription of the gene for IL-2 RECEPTORS...thus decreased expression on surface of helper T cells
***It does the above by binding to cytoplasmic protein on helper T cell (cyclophilin) which inhibits the enzymatic activity of calcineurin
-- calcineurin dephosph NFATC which normally activates genes for IL-2, IL-2 receptors, TNFb, and IFNg
Tacrolimus MOA?
-- bonds to the cytosolic protein FKBP of helper T cells
-- tacrolimus-FKBP complex also inhibits calcineurin and thus prevents production of IL-2, IL-2 receptors, TNFb, and IFNg
Sirolimus (rapamycin) MOA?
Interacts w/ intracellular immunophyllins to block T and B cell activation by cytokines caysing the cells to go into cell cycle arrest.

DOES NOT inhibit IL-2 production by activated T cells
Mycophenolate mofetil MOA?
1. Potent inhibitor of inosine monophosphate dehydrogenase, an enzyme critical in the de novo synthesis of the purine guanine by T and B lymphocytes

2. Acts specifically on lymphocytes b/c these cells, unlike others derived from bone marrow, have no alternative pathway (HGPRT salvage pathway) for purine biosynthesis
Azathioprine MOA?
1. Converted to 6-mercaptopurine which in turn is eventually converted to thio-GTP. This purine analog is incorporated into the DNA where it inhibs further DNA synth and prevents T-cell and B-cell expansion
2. 6-mercaptopurine is cytotoxic and kills stimulated lymphocytes
3. Inhibs prolif of promyelocytes in bone marrow and thus decreases number of circ monocytes capable of differentiation into macrophages
Cyclophosphamide MOA?
1. Alkylation of the 7 nitrogen of guanine causes cross-linking of the DNA strands which inhibits DNA replication and translocation

2. Interferes w/ mitosis and division in rapidly proliferating cells, thus causing cell death
OKT3 (muromonab-CD3) MOA?
Monoclonal Ab (produced by hybridomas)
1. Ab is directed against CD3 complex of T helper cells and cytotoxic T cells
2. CD3 protein lies right next to Ag-recognition cmplx of helper T cell receptor
3. Binding to the CD3 complex blocks binding of the foreign Ag presented by the APC; helper T cell cannot be activated to produce IL-2, etc.
4. Deactivation of the CD3 complex causes Tcell receptor Ag recognition site to endocytose
5. Fxn of cytotox T cells is blocked
6. T cells become inactive and are removed from circ by reticuloendothelial system