Preformed recipient's antibody reacts w/ donor's antigen and complement 

Time for suppression= minutes to hours 

Antigen activates recipient's T cells, recipient generates antibodies against donot antigen

Time for suppression= weeks to months

Thought to be chronic inflammation resulting from T cell responses to donor antigen 

Time for suppression: months to years 

Clonal deletion of autoreactive T and B cells during developmental stage 

so that majority of immature T and B cells do not develop into self-reeactive clones

- Acute rheumatic fever

- Autoimmune hemolytic anemia

- Goodpasture's syndrome 

False, this is acute rheumatic fever 

Autoimmune hemolytic anemia has Rh group antigen (autoantigen) and result is destruction of erythrocytes 

Autoantigen= Renal glomerular basement membrane collagen type IV

Result: glomerulonephritis, pulmonary hemorrhage 

- Mixed essential cryoglobulinemia: autoantigen= rheumatoid factor IgG complexes, result systemic vasculitis 

- Systemic lupus erythematosus: autoantigen= DNA, histones, ribosomes, snRNP, scRNP, result glomerulonephritis vasculitis, arthritis 

- Multiple sclerosis: autoantigen= myelin oligodendrocyte glycoprotein, result CNS deficit

- Rheumatoid arthritis: Unknow autoantigen-possible synovial antigens, result joint inflammation and destruction 

- Rheumatoid arthritis

- Psoriasis

- Scleroderma

- Systemic lupus

- Erythematosus

- Multiple sclerosis

- Myasthenia gravis, crohn's disease, grave's disease, type 1 diabetes 

Anti CD3: muromonab

Anti-CD20 mAb: rituximab

Anti-CD25 mAb: basiliximab 

Efalizunab

Natalizumab

GI (most commons): ulcerative stomatitis, nausea, abd pain

Low white blood cell count and thus predisposition to infection (acute penumonitis)

Highly teratogenic (pregnancy X)

Pulmonary toxicity, liver toxicity, renal toxicity 

Pts w/ liver disease or renal disorders

Pts with blood disorders

Pts with peptic ulcers or ulcerative colitis

Pregnancy

NSAIDs increase methotrexate blood levels (plasma protein displacement, and inhibit elimination)

Sulfas, tetracycline, phenytoin, can also displace methotrexate 

N/V, diarrhea abd pain

Myelosuppression (leukopenia, neutropenia)

Increased risk of infection

Lymphoma 

DI= Iron recudes MMF oral bioavailability 

False, it inhibits de novo synthesis 

its derivative of mercaptopurine, prevents clonal expansion of both B and T lymphocytes

- Skin rashes

- GI effects

- Liver toxicity

- Bone marrow suppression 

DHFR

Methotrexate exerts greater toxic effect on rapidly dividing maligant and myeloid cells 

Even w/ lower dose SE as hair loss, nausea, HD, and skin pigmentation still common 

Which of the followings are correct for leflunomide?

I) Decrease DNA, RNA, & protein synthesis

II) decrease proinflammatory cytokines

III) increase lymphocyte proliferation

IV) decrease B & T cell propulation

A) I only

B) I, II, III

C) I,II,IV

D) all of the above 

C) I, II, IV 

III) decrease lymphocyte proliferation 

Inhibitor of T-cell mediated immunity

Inhibit production of IL-2 by activated T cells 

False, it's more potent

Everything else is correct 

Block IL-2 receptor signaling required for T cell proliferation 

It structurally similar to tacrolimus but has different MOA 

True 

NFAT will translocate and IL-2 production is suppressed 

Binds to FKBP and the formed complex binds to mTOR (molecular target of rapmycin (sirolimus)), it blocks the progression of activated T cells from G1 to S phase of cell cycle, thus blocks T cell response to cytokines

It also inhibits B cell proliferation and immunoglobulin production 

- Nephrotoxicity

- Neurotoxicity

- Hepatotoxicity

- Hyperlipedemia 

- HTN

- Infection

- Gigival

- Hyperplasia, GI disturbance, hirsutism 

Hepatotoxicity, HTN, peripheral edema, thrombolic disorder, hyperlipedimia, anemia, thrombocytopenia, arthralgia, lymphoma and infection

NO nephrotoxicity

- CYP 450 inducers; phenobarbitone, phenytoin, rifampin, st john's wort, enhance clearance of cyclosporine resulting rejection of transplant

- Erythromycin, ketoconazole, grapefruit juice drecrease cyclosporine clearance and increase risk of cyclosporine toxicity 

- Rheumatoid arthritis

- Juvenile rheumatoid arthritis

- Plaque psoriasis

- Psoriatic arthritis

- Ankylosing spondylitis

- Rheumatoid arthritis

- Crohn's disease

- Ulceratvie colitis

- Ankylosin spondylitis

- Rheumatoid arthritis

- Psoriatic arthritis 

- Myelosuppression

- Heart failure

- Optic neuritis

- TB reactivation

- Increased risk of infection

- Injection site reaction

- Upper respiratory infection

- Abd pain, vomiting 

Polyclonal rabbit antibody. Bind to cell surface molecules and block lymphocyte function. deplete circulating lymphocytes by direct citotoxicity is MOA of which antibody?

a) muromonab-CD3

b) Rituximab

c) Anti-thymocyte globulin (ATG)

It 's a partially huminized anti-CD20 antibody. Depletes circulating B cells is MOA of which antibody?

a) Rituximab

b) daclizumab

c)anti-thymocyte globulin (ATG)

d) Alefacept

False, this is MOA of alefacept

Alemtuzumab is an anti-CD52 mAb, it causes apoptosis of lymphocytes and monocytes 

False, CTLA-4 fused to an Ig1 constant region

the cells develops anergy or undergo apoptosis 

exacerbation of astham and susceptibility to infection

Which drug limits T cell adhesion, activation and migration to sites of action by disrupting integrin and ICAM-1 interaction?

a) abatacept

b) Efalizumab

c) Ritixumab

d) Alefacept

b) efalizumab it is a mAb against LFA-1, an integrin that binds ICAM-1 

It does not eradicate the cells