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42 Cards in this Set

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Question: What immune cell recognizes foreign peptides bound to MHC II on the surface of APC cells, secretes IL-2, and initiates the cell-mediated immunity reaction responsible for host-versus-graft reactions?
Th cells
Question: Cyclosporine is effective in organ transplantation. What is its MAO?
inhibition of the gene transcription of interleukins.

Cyclosporine inhibits calcineurin, a serine phosphatase that is needed for activation of T-cell specific transcription factors. Gene transcription of IL-2, IL-3, and INF-gamma
Question: What is a widely used drug that suppresses cellular immunity, inhibits prostaglandin and leukotriene synthesis, and increases catabolism of IgG?
Prednisone
Question: Leukocyte-activated killer cells (LAKs) are cytotoxic across MHC barriers and can even kill cells that do not express MHC. What drug activates LAKs?
Aldesleukin, a recombinant IL-2.

Used for renal cell carcinoma, malignant melanoma, and restoring immune function in AIDS.
Question: What drug is used to prevent primary immune response of an Rh-negative mother to an Rh-positive newborn?
Rho(D) immune globulin.

Administer within 72 h after birth of a Rh+ infant to a Rh- mother.
Question: What monoclonal AB binds to TNF-alpha and inhibits its actions?
Infliximab.

Etanercept also binds to TNF-alpha, but is a chimeric protein containing a portion of human TNF-alpha receptor linked to the Fc region of human IgG.

Thalidomide inhibits production of TNF-alpha
Question: PT treated with penicillin develops bronchoconstriction, laryngeal edema, and hypotension. He survives from EPI. He is treated a year later with an antipsychotic drug and develops agranulocytosis.

What is the process triggered by both penicillin and by the antipsychotic drug?
Penicillin caused a type 1 drug reaction mediated by IgE ABs.

Agranulocytosis and SLE are type II drug reactions involving IgM and IgG ABs that bind to circulating blood cells.
Question: What immunosuppressant suppresses both B- and T-cells via inhibition of de novo synthesis of purines?
Mycophenolate mofetil

Forms into mycophenolic acid that inhibits inosine monophosphate dehydrogenase, the rate-limiting enzyme in the de novo pathway of purine synthesis.
Question: Recombinant IL-2 has proved useful in what?
IL-2 stimulates T-cell proliferation and activates Th1, NK, and LAK cells.

Efficacy in renal cell carcinoma, malignant melanoma, 2 cancers that respond poorly to conventional cytotoxic anticancer drugs.
Question: Although sirolimus and cyclosporine have similar immunosuppressant effects, what toxicity is associated with sirolimus rather than cyclosporine?
Cyclosporine and tacrolimus are both associated with renal toxicity and hypertension.

Sirolimus appears to spare the kidney and cause GI disturbances, hypertriglyceridemia, and myelosuppression, especially in the form of thrombocytopenia.
Question: What immune modulator increases phagocytosis by macropahges in PTs with chronic granulomatous disease?
TNF-gamma
The critical inaugural step in adaptive immune response involves?
Antigen-presenting cells, which process antigens into small peptides that are recognized by CD4
Activated Th cells secrete what, and what is that product roll?
IL-2 that initiates proliferation and activation of Th1 and Th2.
What is the function of Th1?
Participate in cell-mediated and delayed hypersensitivity.

They produce IFN-gamma, IL-2, TNF-beta (aka lymphotoxin). These cytokines activate macrophages, CD8, CTLs, and NKs
How is the humoral response triggered?
When B cells bind antigen via their surface Ig, the antigen is internalized and the peptides are displayed on the MHC II. When the T-receptors on Th2 are activated by the MHC II-peptide complex, they secrete cytokines to induce B-cell proliferation and differentiation into memory B cells and AB-secreting plasma cells.
What is the MOA of ABs?
Trigger the precipitation of viruses and destruction of bacteria by phagocytic cells or lysis by the complement system.
IL-10 and IFN-gamma downregulate what?
Th1 and Th2 respectively.
Immediate hypersensitivity, delayed hypersensitivity, and autoimmunity arise from?
AB-mediated, cell-mediated, and self-reactive lymphocytes respectively.
What is the MOA of corticosteroids?
Decrease synthesis of prostaglandins, leukotrienes, cytokines, and other signaling molecules (eg, platelet activating factor).

Inhibit the proliferation of T-cells and are cytotoxic to certain T cells; therefore, the humoral immunity is also dampened and continuous therapy lowers IgG levels.
What are the SE of corticosteroids?
Adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt retention, glucose intolerance, and behavioral changes
What is the MOA of immunosuppressants?
They interfere with T-cell function by binding to immunophilins, small cytoplasmic proteins that play critical roles in T-cell responses to T-cell receptor activation and to cytokines.
What do cyclosporine and tacrolimus bind to? What do they both result in?
Cylcosporine binds to cyclophilin. Tacrolimus binds to FK-binding protein (FKBP)

Both inhibit calcineurin, a cyclophatase that regulates the ability of nuclear factor of activated T cells (NFAT) to translocate to the nucleus and increase the production of key cytokines IL-2, IL-3, and IFN-gamma.
What does sirolimus bind to, and how is it different than tacrolimus?
Inhibits calcineurin by binding to FKBP; however, this proliferation signal inhibitor interferes with the response of T cells to cytokines without affecting cytokine production.

Also appears to inhibit B-cell proliferation and AB production.
In addition for providing treatment in solid organ transplantation and graft-versus-host, what else is cyclosporine and tacrolimus, as well as Sirolimus used for?
Cyclosporine and tacrolimus: autoimmune diseases, such as rheumatoid arthritis, uveitis, psoriasis, asthma, and T1DM

Sirolimus-eluting stents: used to prevent restenosis after coronary angioplasty.
What are the SE associated with cyclosporine and tacrolimus? And sirolimus?
Cyclosporine and tacrolimus: nephrotoxicity, hypertension, neurotoxicity. Can also cause hyperglycemia, hyperlipidemia, and cholelithiasis.

Sirolimus: more likely than the above to cause hyperlipidemia, thrombocytopenia, leukopenia (myelosuppression).
What is the MOA of mycophenolate mofetil? What is the consequence?
Converted into mycophenolic acid, which inhibits inosine monophosphate dehydrogenase, an enzyme involved in the de novo pathway of guanosine triphosphate (GTP) synthesis.

This suppression both B- and T-cell activation.

Note: lymphocytes lack enzymes for the salvage pathway of GTP synthesis.
What is mycophenolate mofetil used for and its SE?
Immunosuppressant in transplant PTs. Myelosuppression, especially neutropenia.
What is the MOA of thalidomide? Its usage, and its SE. What is the known teratogenic effects associated with this drug?
Reduction of TNF-alpha, increase IL-10, reduced neutrophil phagocytosis, altered adhesion, enhanced cell-mediated immunity.

Erythema nodosum leprae, multiple myeloma.

Sedation, neutropenia, peripheral neuropathy

Limb defects ("flipper" limbs): shortening or absence of limbs.
What is the MOA of alefacept? What is it used for? SE?
Blocks the CD2 receptor. Used for psoriasis. Dose-dependent reduction in circulating T-cells.
What is the MOA of antilymphocyte globulin and antithymocyte globulin? SE?
These ABs bind to T cells involved in antigen recognition and initiate their destruction by serum complement.

These ABs selectively block cellular immunity rather than AB formation, which accounts for their ability to suppress organ graft, a cell-mediated process.

Since the humoral immunity may still be intact, they can cause hypersensitivity reactions, such as serum sickness and anaphylaxis.
What is RhoGAM MOA and what is it used for?
Is a IgG prepration containing ABs against red cell RHo(D) antigens.

For Rho(D)-negative mothers whose child may be RhD+; therefore, preventing Rh hemolytic disease of the newborn.
What monoclonal AB binds to CD3, the consequence, what is it used for, and its SE.
Muromonab blocks the killing action of CTL and is used for transplant rejection crises.

Serious anaphylactic reactions, and neuropsychiatric and hypersensitivity reactions as well.
What is a monoclonal AB against IL-2 receptors? What is it used for?
Daclizumab.

Used in combination with other immunosuppressants to prevent renal transplant rejection.
What is the MOA of infliximab, and what is it used for?
Monoclonal AB TNF-alpha inhibitor.

Crohn's disease, rheumatoid arthritis, ulcerative colitis, ankylosing spondylitis, psoriatic arthritis.
What is adalimumab MOA? What is it used for?
Monoclonal AB TNF-alpha inhibitor

Autoimmune diseases such as rheumatoid arthritis
What is etanercept MOA? What is it used for?
Is not a monoclonal AB, but binds to TNF-alpha with high affinity.

Arthritis, psoriasis, and ankylosing spondylitis.
What is TNF-alpha, and what is its functions?

Inhibitors of TNF-alpha can cause?
A cytokine, produced by macrophages and T cells that stimulates the release of other inflammatory cytokines (IL-1, IL-6, IL-8).

All anti-TNF-alpha agents increase the risk of serious infections and lymphoma.
What is aldesleukin MOA? Used for?
Recombinant IL-2 that promotes the production of CTL and activates NK.

Adjunctive treatment
What is INF-alpha used for? Beta? gamma?
INF-alpha: chronic HBV, HCV, Kaposi sarcoma, melanoma, leukemia

INF-beta: MS

INF-gamma: NADPH oxidase deficiency in chronic granulomatous disease.

Note: INF-gamma has greater immune enhancing actions than other INF and increases the synthesis of TNF.
What is the mechanism behind type I (immediate) drug allergy? What are the features? What drugs are involved?
IgE-mediated reactions.

Anaphylaxis, urticaria, and angioedmea

Penicillins and sulfonamides.
What is the mechanism behind type II drug allergy? What drugs are involved?
Involves IgG or IgM ABs that are bound to circulating blood cells. On reexposure to the antigen, complement dependent cell lysis occurs.

Hemolytic anemia methyldopa, SLE from hydralazine or procainamide, thrombocytopenic pupura from quinidine, and agranulocytosis from many other drugs.
What is the mechanism behind type III drug allergy? What drugs are involved?
Complement fixing IgM or IgG AB, and possiably IgE.

Drug induced serum sickness and vasculitis are examples; Stevens-Johnson syndrome (associated with sulfonamide therapy)