immunosupressant drugs Flashcards
. Which of the following is NOT a primary reason for prescribing immunosuppressive drugs?
A. To treat viral infections that cause immune overactivation
B. To reduce organ rejection following transplantation
C. To treat autoimmune diseases like lupus or rheumatoid arthritis
D. To prevent graft-versus-host disease after bone marrow transplants
A is the correct answer
In graft-versus-host disease (GVHD), the immune response is initiated by:
A. Host immune cells attacking donor tissue
B. Donor immune cells attacking host tissue
C. A deficiency in T-cell production
D. Antibodies binding to host red blood cells
Donor immune cells attacking host tissue
what is an autoimmune disease?
when the host’s immune cells react inappropriately and target the host’s own cells
Which phase of the adaptive immune response is most commonly targeted by immunosuppressive drugs?
A. Innate recognition phase
B. Effector phase
C. Induction phase
D. Memory phase
Induction phase. most immunosuppressant drugs interefere with T-cell activation during the induction phase
induction phase is is the recognition of an antigen and activation of tcells
How is the induction phase and the effector phase key phases for adaptive immunity?
induction phase involves presentation of the foregin antigen by an antigen presenting cell
acttivations and proliferation of naive T-helper cells (Th0) are differentiated into Th1 and Th2
the effector phase involves T-cell responses derived from Th1 cells and antibody responses by Th2 cells these kill the pathogens
what steps of immune responses do imunosupressant drugs target?
target…
- inhibitions of IL-2 production/activation
- inhibitions of cytokine gene expression (glutocorticoids
- cytotoxicity (killing immune cells)
- inhibition of nucleic acid synthesis
- blockage of receptors on T-cell surface
What is the primary function of calcineurin in T-cell activation?
A. It activates cytokine receptors on the T-cell surface
B. It increases antibody production in B cells
C. It dephosphorylates NFAT, allowing it to enter the nucleus
D. It promotes DNA replication in activated T-cells
Calcineurin is a phosphatase that activates NFAT, which then induces IL-2 gene transcription.
what is the importance of IL-2 for naive T-cells and clonal expandion of T-cells?
IL-2 is an important cytokine required for the activation of naives and clonal expansion T-cells
IL-2 is made by proliferating T-cells
note: IL2 is controlled by NFAT pathway
Cyclosporine and tacrolimus both inhibit IL-2 production by:
A. Blocking mTOR signaling in the nucleus
B. Disrupting the IL-2 receptor on B cells
C. Inhibiting calcineurin activity via immunophilin binding
D. Preventing NF-κB activation through glucocorticoid mimicry
Both drugs form complexes with immunophilins (cyclophilin/FKBP) that block calcineurin.
what drugs are examples of calcineurin inhibitors?
cyclosporin and tacrolimus
how does calcinuerin, IL-2, and NFAT relate?
T-cell receptor activation triggers a calcium (Ca²⁺) signal.
This activates calcineurin, a phosphatase enzyme. (calineurin=switch)
Calcineurin dephosphorylates NFAT (Nuclear Factor of Activated T-cells).
Once dephosphorylated, NFAT translocates to the nucleus. (control room)
Inside the nucleus, NFAT drives transcription of the IL-2 gene.
IL-2 is a key cytokine that promotes T-cell multiplication, helping immune response
how does cyclosporin and tacrolimus work differently?
cyclosporin inhibit calcineurin by cyclophilin (cyclosporin complex)
- prevents NFAT gene transcription of IL-2, no more T-cell proliferation and migration
tacrolimus:
- binds to the FKB tacromilus complex, this inhibits calcineurin
- no NFAT to turn on IL-2 gene
- both are calineurin inhibitors
Which drug forms a complex with FKBP but does NOT inhibit calcineurin? what does it inhibit instead?
A. Tacrolimus
B. Cyclosporine
C. Rapamycin
D. Alemtuzumab
Rapamycin
Rapamycin binds FKBP but targets mTOR, not calcineurin.
*Mtor is a major pathway thats reponsible to promote cell growth and proliferation
a drug that interferes witht the downstream signals of IL-2 receptor activation. it is also a proliferating agent
rapamycin
which is true about FKBP?
1. it is an FK406 binding protein
2. it is an FK506 binding protein
3. they target beta receptors
4. they help cytokines and other proteins fold
5. they are cis-trans isomerases
6. its what cyclosporin and tacromilus make a complex out of
7. its what rapamycin binds to
it is an FK506 binding protein
its a peptidyl proline cis-trans isomerases (protein folding chaperones)
they help cytokines fold
FKBP’s target calcineurin (protein phosphatase), mTOR, ryanadine receptors and Ip3 receptors
its what rapamycin binds to
Why are cytotoxic agents like azathioprine effective as immunosuppressants?
A. They block surface receptors required for antigen presentation
B. They directly degrade IL-2, halting T-cell activation
C. They mimic nucleotides and disrupt DNA synthesis in dividing cells
D. They suppress phagocytosis by interfering with Fc receptors
They mimic nucleotides and disrupt DNA synthesis in dividing cells
Azathioprine is metabolized into 6-MP, a fraudulent nucleotide, disrupting purine synthesis.
what is the difference between the mTOR pathways and the calineurin pathway
mTOR= pathway that is important for promoting cell growth
calineurin path: plays a role in T-cell activation and proliferation, leads to expression of IL-2
cyclophosphamide and azathioprine are examples of…
cytotoxic agents
how do cytotoxic agents cyclophosphamide and azathioprine differ?
cyclophosphamide cross links neighbouring DNA, affecting cell division and proliferation
azathioprine is metabolized to mecaptopurine which is a fraudulent nucleotide (a nucleotide that is missing something important in the structure, which inhibits synthesis)
-it also inhibits nucleotide synthesis
Which enzyme is inhibited by 6-mercaptopurine, leading to suppression of purine synthesis?
A. mTOR
B. Calcineurin
C. PRPP amidotransferase
D. IL-2 kinase
PRPP (phophoribosyl pyrophosphate amuditransferase)
which is a purine analog
6-MP inhibits PRPP amidotransferase, blocking purine nucleotide biosynthesis.
what is the difference between the Fab sections and the Fc section of the antibody?
Fab is for antigen binding and specifity
Fc is for determining the anti-bodies class and cell response(IgA, IgG, IgM, etc)
- also a crystallizable fragment
which is true about antibodies?
a. they consit of 4 polypeptide chains
b. they have 4 identicle heavy chains
c. they have 4 identicle light chains
d. they have two identicle light chains and two identicle heavy chains
they consit of 4 polypeptide chains
hey have two identicle light chains and two identicle heavy chains
section of the antibody used to identify antibody class and makes a cell response to that correlating antibody
the Fc fragment
What is a major reason for using humanized or chimeric monoclonal antibodies instead of mouse-derived ones?
A. Mouse antibodies do not bind to human antigens
B. They are less effective at activating complement
C. Mouse antibodies have shorter half-lives and provoke immune responses
D. Chimeric antibodies are cheaper and easier to produce
Mouse antibodies are recognized as foreign, so they are quickly degraded and can trigger immune responses.
Mouse antibodies have shorter half-lives and provoke immune responses
