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193 Cards in this Set

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Lymph node - functions
Non-specific filtration by Macs
Storage and activation B/T cells
Antibody production
Lymph node follicle
Site of B-cell localization and proliferation
Located in outer cortex

Primary follicle: Dense and dormant
Secondary follicle: pale central germinal centers and are active
Lymph node medulla
Medullary cords: Plasma cells

Medullary sinuses: Macs and reticular cells
Lymph node paracortex
Houses T-cells
Region of cortex between follicles and medulla

Paracortical hyperplasia in extreme cellular immune response (i.e. viral--EBV)

Not well developed in DiGeorge's syndrome
Lymph node drainage

Upper limb, lateral breast
Axillary
Lymph node drainage

Stomach
Celiac
Lymph node drainage

duodenum, jejunum
Superior mesenteric
Lymph node drainage

Sigmoid colon
Colic --> Inferior Mesenteric
Lymph node drainage

Rectum (lower part)
Anal canal (above pectinate line)
Internal Iliac
Lymph node drainage

Anal canal below pectinate line
Superficial inguinal
Lymph node drainage

Testes
Superficial and deep plexus --> para-aortic
Lymph node drainage

Scrotum
Superficial inguinal
Lymph node drainage

Superficial Thigh
Superficial inguinal
Lymph node drainage

Lateral side of dorsum of foot
Popliteal
Lymph node drainage

Right arm and right half of head
Right lymphatic duct
Thoracic duct drainage
collects most of the lymph in the body

drains into the systemic (blood) circulation at the left brachiocephalic vein, between where the left subclavian vein and left internal jugular connect
Sinusoids of the spleen
Long, vascular channels in red pulp with fenestrated "barrel hoop" BM.

Macs found nearby.
T-cells in the spleen
Found in the PALS (periarterial lymphatic sheath) and red pulp
B-cells in the spleen - location
Follicles within the white pulp
Red pulp of the spleen - function
Mechanical filtration of RBCs

Reserve of monocytes
White pulp of the spleen - function
Active immune response through humoral and cellular pathways

Antibody production
What removes encapsulated bacteria in the spleen?
Macrophages
Mechanism of infxn susceptibility in splenic dysfunction/asplenia
Decreased IgM --> decreased C3b opsonization --> increased susceptibility to encapsulated organisms
Organisms of concern in splenectomized patients
S. pneumoniae
H. influenzae
Salmonella
N. Meningitidis
Blood smear results post-splenectomy
Howell-Jolly bodies
Target cells
Thrombocytosis
Sites of T and B-cell maturation
T: thymus

B: bone marrow
Thymus: Structural Organization and Function
Encapsulated. Cortex and medulla.

Site of T-cell differentiation and maturation.
Where is the thymus embryologically derived from?
3rd branchial pouch.
Thymus: cortex and medulla

Cellular histology
Cortex: dense with immature T-cells

Medulla: pale with mature T-cells and epithelial reticular cells, contains Hassall's corpuscles

Corticomedullary junction: where + and - selection occur
Thymocyte maturation process:
Occurs at corticomedullary junction

1. Immature thymocytes from BM make T-cell receptors by gene rearrangement

2. + selection (MHC restriction) for functional T-cells occurs in the cortex

3. - selection for autoreactive T-cells occurs in the medulla
Innate Immunity
Receptors that recognize pathogens are germline encoded.

Response to pathogens is fast and non-specific.

PMNs, Macs, Dendritic cells, NK cells and complement
Adaptive Immunity
Receptors that recognize pathogens undergo VDJ recombination during development.

Response is slow on 1st exposure, but memory response is faster and more robust.

T-cells, B-cells, and circulating Ab
Cytotoxic T-cell: function
CD8+

kills virus infected, neoplastic and donor graft cells
Helper T-cell:

Types and functions
CD4+

IL-12 --> Th1 Cell (cell-mediated response)

IL-4 --> Th2 Cell (humoral response)
Th1 cell function
CD4+ --> Cell mediated response

Make IL-2, IFN-g
Activate Macs and CD8+ cells
Inhibited by IL-10
Th2 Cell function
CD4+ --> Humoral response

Make IL-4, IL-5, IL-10
Helps B-cells make Abs
Inhibited by IFN-g
MHC
Encoded by HLA genes

Present Ag fragments to T-cells and binds TCR
MHC I
HLA-A, HLA-B, HLA-C

Expressed on almost all nucleated cells.
Ag is loaded on RER of most intracellular peptides.
Mediates viral immunity.
Pairs with B2-microglobulin (aids in transport to cell surface)
MHC II
HLA-DR, HLA-DP, HLA-DQ

Expressed only on APCs.
Ag is loaded following release of invariant chain in an acidified endosome.
HLA-A3
Hemochromatosis
HLA-B27
PAIR

Psoriatic arthritis
Ankylosing spondylitis
IBD
Reiter syndrome
HLA-B8
Grave's Disease
HLA-DR2
MS
Hay fever
SLE
Goodpasture's
HLA-DR3
DM Type 1
HLA-DR4
RA
DM Type 1
HLA-DR5
Pernicious anemia (B12 deficiency)
Hashimoto's thyroiditis
HLA-DR7
Steroid-responsive nephrotic syndrome
B-cell functions
Make Ab
IgG: opsonize bacteria, neutralize viruses

Hypersensitivity rxns:
Type I: IgE, allergy
Type II: IgG/IgM, cytotoxic and Ab dependant
Type III: IgG, immune complex deposition

Preformed Abs can cause hyperacute organ rejection
T-cell functions
CD4+: T-cells help B-cells make Ab and produce gamma interferon (activates Macs)

CD8+: Directly kills virus infected cells

Type 4 Hypersensitivity: delayed cell-mediated

Acute and chronic organ (allograft) rejection
NK Cells
Only lymphocyte member of innate immunity

Uses perforin and granzymes to induce apoptosis of virally infected cells and tumor cells

Activity is enhanced by IL-12, IFN-B, IFN-a
What induces NK cells to kill?
When exposed to:

1) Non-specific activation signal on target cell
2) absence of MHC I on target cell surface
T-cell glycoproteins
CD4: binds MHC II
CD8: binds MHC I
CD3 complex: cluster associated with T-cell receptor

Important in signal transduction
3 Antigen Presenting Cells
Macs
B-cells
Dendritic cells
Macrophage-lymphocyte interactions
Activated lymphocytes and macrophages stimulate one another

Lymphocytes secrete IFN-g --> Macs

Macs secrete IL-1, TNFa --> lymphocytes
Effect of superantigens (S.pyogenes and S.aureus)
cross-link B-region of TCR to MHC II on APCs

results in uncoordinated release of IFN-g from Th1 cells and subsequent release of IL-1, IL-6 and TNF-a from Macs
Effects of endotoxin/LPS from gram(-) bacteria
directly stimulate Macs by binding to endotoxin receptor CD14
Th cell activation
Signal 1: foreign antigen (phagocytosed by APC) is presented on MHC II and recognized by TCR on Th cell

Signal 2: "Costimulatory signal" is given by interaction of B27 (APC) and CD28 (Th)

Th cell is now activated to produce cytokines
Tc cell activation
Signal 1: Endogenously synthesized (viral or self) proteins presented on MHC I and recognized by TCR on Tc cell

Signal 2: IL-2 from Th cell activates Tc cell to kill virus infected cell
B-cell class switching
Signal 1: IL-4, IL-5, IL-6 from Th2 cell

Signal 2: CD40 receptor activation by binding CD40L on Th cell
Antibody structure
Variable part of L and H chains recognize Ag

Fc portion of IgM and IgG fixes complement

Heavy chain: Contributes to Fc and Fab fractions
Light chain: Contributes only to Fab fraction

Chains held together by disulfide bonds
Fab
Ag binding fragment

Determines idiotype: only 1 antigenic specificity expressed per B-cell type
Fc
Constant
Carboxy terminal
Complement binding (IgG and IgM)
Carbohydrate side chains

Determines Isotype (IgM, IgD, etc)
Functions of Abs
Opsonization: promotes phagocytosis

Neutralization: prevents bacterial adherence

Complement activation: activates complement, enhancing opsonization and lysis
Ab diversity is generated by:
1. random recombination of VJ (light-chain) or V(D)J (heavy) chain genes

2. Random combination of heavy chains with light chains

3. Somatic hypermutation (following stimulation)

4. Addition of nucleotides to DNA during recombination by terminal deoxynucleotide transferase
B-cell isotype switching
Alternative splicing of mRNA, mediated by cytokines and CD40L

Mature B-cells express IgM and IgD on surfaces

Can differentiate by isotype switching into plasma cells that secrete IgA, IgE or IgG
IgG
Main Ab in secondary (delayed) response to Ag.
Most abundant.

Fixes complement
Crosses placenta (provides passive immunity in infants)
Opsonizes bacteria
Neutralizes bacterial toxins and viruses
IgA
Prevents attachment of bacteria and viruses to mucous membranes.

Does not fix complement.
Found in secretions (saliva, tears, mucus) and breast milk (colostrum)
IgM
Produced in the primary (immediate) response to an antigen.

Fixes complement
Does not cross the placenta
Antigen receptors on the surface of B-cells
IgM and IgG
IgD
Unclear function.

Found on surface on many B cells and in serum.
IgE
Binds mast cells and basophils.

Cross links when exposed to allergen, mediating Type I (immediate) hypersensitivity through release of histamine.

Mediates immunity to worms by activating eosinophils.

Lowest concentration in serum.
Ig Allotype
Polymorphism - Ig epitope that differers among members of the same species.

Can be on light or heavy chain.

ALLotypes represent different ALLeles.
Ig Isotype
Ig epitope common to a single Ig class.

Ig MADGE
Ig Idiotype
Specific for a given antigen. Ig epitope determined by Ag-binding sites.

Hypervariable region is unique.
Thymus-independent Ag
Antigens lacking a peptide component.
Cannot be presented by MHC to T-cells.
Stimulate release of IgM Abs only and do not result in immunologic memory.

Ex: LPS from cell envelope of gram (-) bacteria and polysaccharide
Thymus-dependent Ag
Ag containing a peptide component.

Class switching and immunologic memory occur as a result of direct contact with Th cells (CD40-CD40L interaction).

Release of IL-4, IL-5, IL-6.

Ex: H.influenzae vaccine
IL-1
Secreted by Macs --> acute inflammation.

Recruit leukocytes
Activates endothelium to express adhesion molecules

Endogenous pyrogen
IL-2
Secreted by Th cells.

Stimulates growth of helper and cytotoxic T-cells.
IL-3
Secreted by activated T-cells.

Growth and differentiation of bone marrow stem cells. (Similar to GM-CSF)
IL-4
Secreted by Th2 cells.

Growth of B-cells.
Enhances class switching to IgE and IgG.
IL-5
Secreted by Th2 cells.

Differentiation of B-cells.
Class switching to IgA.
Production/activation of IgE.
IL-6
Secreted by Th cells and Macs.

Production of acute phase reactants and Ig's.
IL-8
Secreted by Macs.

Major chemotactic factor for PMNs.
Help clear infxns.

"Clean up on aisle 8"
IL-10
Secreted by regulatory T-cells.

Inhibits actions of activated T-cells.
Activates Th-2, inhibit Th-1.
IL-12
Secreted by B-cells and Macs.

Activates NK cells and Th1 cells.
Gamma interferon
Secreted by Th1 cells.

Stimulates Macs. Activates Th1, inhibits Th2.
TNF
Secreted by Macs.

Septic shock.
Leukocyte recruitment, vascular leak.
Hot T-Bone stEAk
IL-1: hot (fever)
IL-2: stimulate T-cells
IL-3: stimulate bone marrow
IL-4: stimulate IgE production
IL-5: stimulate IgA production
Helper T-cells - cell surface proteins
CD4
CD3
CD40L

CD28
TCR
Cytotoxic T-cells - cell surface proteins
CD8
CD3

TCR
B-cells
IgM
MHC II
CD40
CD19
CD20

CD21 (receptor for EBV)
B7
Macrophages - cell surface proteins
MHC II
CD40
B7

CD14
Receptors for Fc, C3b
NK cells
Receptors for MHC I
Receptor for Fc of IgG

CD56
All cells except mature RBCs
MHC I
Interferon mechanism
Proteins that place uninfected cells in anti-viral state.

Induce production of a ribonuclease that inhibits viral protein synthesis by degrading viral mRNA.

"Interferes with viruses"
Interferon functions
1. alpha and beta: inhibit viral protein synthesis.

2. gamma: increase MHC I and II expression and Ag presentation in all cells

3. activates NK cells to kill virus-infected cells
Active immunity
Induced after exposure to a foreign antigen.

Slow onset.

Long acting protection -- memory.
Passive immunity
Receiving pre-formed Abs from another host.

Rapid onset. Short life-span of Abs (3 weeks).

Ex: IgA in breast milk.
Which toxins require the administration of preformed (passive) Abs?
Tetanus
Botulinum
HBV
Rabies

"After exposure to Tetanus, Botulinum, HBV, Rabies, patients are given pre-formed Abs To Be Healed Rapidly"
Complement system
System of proteins that interact to play a role in humoral immunity and inflammation.
MAC defends against what type of bacteria?
Gram negative
Classic pathway (complement)
Activated by complement proteins binding antigen-Ab complexes

IgM or IgG
Alternative pathway (complement)
Activated by complement binding to molecules on microbial surfaces (non-specific activators, i.e. endotoxin)
Mannose-lectin pathway
Activated by mannose-binding lectin binding microbial surfaces
C3b
Main function is opsonization.

Aids in clearance of immune complexes.

Increases internalization by phagocytic cells by opsonization.
2 primary opsonins in bacterial defense
C3b and IgG
Which 2 molecules help prevent complement activation on self-cells?
DAF (decay-accelerating factor)

C1 esterase
Complement proteins involved in viral neutralization
C1 - C4
Complement proteins involved in anaphylaxis
C3a and C5a
C5a
Anaphylaxis and PMN chemotaxis
Membrane Attack Complex is comprised of which complement proteins?
C5b - C9

Function: Lysis and Cytotoxicity
Deficiency of C1 esterase
hereditary angioedema

C1 esterase inhibits C1, F12, kallikrein --> increased vasoactive substances
Hereditary angioedema
C1 esterase deficiency
Deficiency of C3
Severe, recurrent pyogenic sinus and respiratory infxns

Increases susceptibility to type III hypersensitivity rxns
Deficiency of C5-C8
Neisseria bacteremia
Susceptibility to Neisseria bacteremia
Deficiency of C5-C8
Deficiency of DAF
Complement-mediated lysis of RBCs and PNH
Complement mediated lysis of RBCs and PNH
Deficiency of DAF
Antigenic variation in Influenza virus
Major = shift --> "shit"

Minor = drift
Some mechanisms for antigenic variation:
DNA rearrangement

RNA segment reassortment (influenza major shift)
Examples of antigenic variation in bacteria:
Salmonella (2 flagellar variants)

Borellia (relapsing fever)

Parasites (trypanasomes --> programmed rearrangement)
Anergy
Self-reactive T-cells become non-reactive without co-stimulatory molecule.

B-cells also become anergic, but tolerance is less complete than in T-cells.
Granulomatous diseases (8)
1. TB
2. Fungal infxns
3. Syphillis
4. Leprosy
5. Cat scratch fever
6. Sarcoidosis
7. Chron's
8. Berylliosis
Granulomatous disease process
APC induces Th cell to release IFN-g

IFN-g induces monocyte --> Mac --> epithelioid cell --> giant cell
granuloma
giant cell
epithelioid cell
fibroblasts
lymphocytes
Type I Hypersensitivity
Anaphylactic and atopic - First and fast

Free Ag cross-links IgE on presensitized mast cells and basophils --> trigger release of vasoactive amines that act at post-capillary venules

Rapid rxn after Ag exposure due to preformed Ab

Test: Scratch test and radioimmunoabsorbent assay
Type II Hypersensitivity
Antibody mediated.

IgM, IgG bind to fixed Ag on cell --> lysis (via complement) or phagocytosis

Ab and complement lead to MAC

Test: Direct and indirect Coomb's
3 mechanisms of Type II hypersensitivity rxn
1. Opsonize cell or activate complement

2. Ab recruits PMNs and macs that incite tissue damage

3. Bind to normal cellular receptors and interfere with functioning
Type III Hypersensitivity
Immune Complex

Ag-Ab (IgG) complexes activate complement --> attracts PMNs to release lysosomal enzymes.

Immune complex = Ab-Ag-complement

Ex: serum sickness and arthus rxn
Which hypersensitivity types are Ab mediated?
Type I, II, III
Serum Sickness
Type III hypersensitivity

Abs to foreign proteins are produced (5 days).
Immune complexes form and are deposited in membranes, where they fix complement --> tissue damage

Now caused mostly by drugs --> fever urticaria, arthalgias, proteinuria, lymphadenopathy 5-10 days after Ag exposure.
Arthus rxn
Type III hypersensitivity

local subacute Ab-mediated rxn
Intradermal injection of Ag induces Ab --> form Ag-Ab complexes in skin

Sx: edema, necrosis, and activation of complement

Test: Immunofluorescent staining
Type IV Hypersensitivity
Delayed (T-cell mediated) type

Sensitized T-cells encounter antigen and release lymphokines --> Mac activation (no Ab involved)

Not transferable by serum.

4 T's :

T-cells
Transplant rejection
TB skin test
Touching (contact dermatitis)

Test: patch test (i.e. PPD)
4 Hypersensitivity Rxns:
ACID

Anaphylactic and Atopic (I)
Cytotoxic (Ab-mediated) (II)
Immune Complex (III)
Delayed (cell-mediated) (IV)
Type I Hypersensitivity: Disorders
Anaphylaxis (bee sting, food/drug allergies)

Allergies and atopic disorders (i.e. rhinitis, hay fever, eczema, hives, asthma)
Type I Hypersensitivity: Presentation
Immediate, anaphylactic, atopic
Type II Hypersensitivity: Disorders
Hemolytic anemia
Pernicious anemia
ITP
Erythroblastosis fetalis
Acute hemolytic transfusion rxns
Rheumatic fever
Goodpasture's syndrome
Bullous pemphigoid
Pemphigus vulgaris
Grave's disease
Myesthenia gravis
Type III Hypersensitivity: Disorders
SLE
RA
Polyarteritis nodosa
Post-streptococcal glomerulonephritis
Serum sickness
Arthus rxn (i.e. after tetanus vaccine)
Hypersensitivity pneumonitis (i.e. farmer's lung)
Type IV Hypersensitivity: Disorders
DM Type I
MS
Guillan-Barre syndrome
Hashimoto's thyroditis
GVHD
PPD (test for TB)
Contact dermatitis (poison, nickel)
ANA, anti-dsDNA, anti-Smith
SLE
Anti-histone
drug induced lupus
Anti-IgG
aka rheumatoid factor

RA
Anti-centromere
CREST/Sceleroderma
Anti-Scl-70 / anti-DNA topo I
Diffuse scleroderma
Anti-mitochondrial
Primary Biliary Sclerosis
Anti-gliadin, anti-endomysial
Celiac disease
Anti-basement membrane
Goodpasture's syndrome
Anti-desmoglein
Pemphigus vulgaris
Anti-microsomal, anti-thyroglobulin
Hashimoto's thyroiditis
Anti-Jo-1
Polymyositis
Dermatomyositis
Anti-SS-A / anti-Ro

Anti-SS-B/ anti-La
Sjogren's syndrome
Anti-U1 RNP

(ribonucleoprotein)
Mixed connective tissue disease
Anti-smooth muscle
Autoimmune hepatitis
Anti-glutamate decarboxylase
Type I DM
c-ANCA
Wegener's granulomatosis
p-ANCA
other vasculitides
Bruton's aggamaglobulinemia
X-linked recessive
Defect in BTK (tyrosine kinase gene)
Defect in B-cell differentiation/maturation

Recurrent bacterial infxns after 6 mo (decreased maternal IgG)
Opsonization defect

Labs:
Normal pro-B
Decreased B-cells, Ab (all classes)
Hyper-IgM syndrome
Defective CD40L on Thelper cells --> unable to class switch B-cells

Severe pyogenic infxns early in life

Labs:
Increased IgM
Decreased all other Ig's
Selective Ig deficiency
Defect in isotype switching --> specific class of Ig deficiency

Sinus and lung infxns
Milk allergies and diarrhea
Anaphylaxis (after exposure to blood products with IgA)

Labs:
IgA deficiency most common
Thymic aplasia
22q11 deletion --> DiGeorge's
failure to develop 3rd and 4th pharyngeal pouches

tetany (hypocalcemia)
recurrent viral/fungal infxns (T-cell deficient)
congenital heart and great vessel defects

Labs:
Absent thymic shadow in CXR
Decreased T-cells, PTH, Ca
Di George's Symptoms
CATCH

Cardiac anomalies (Tetralogy of Fallot)
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcemia
IL-12 receptor deficiency
Decreased Th1 response

Disseminated mycobacterial infxns

Labs: Decreased IFN-g
Hyper-IgE syndrome
(Job's syndrome)
Th cells fail to produce IFN-g
PMNs unable to respond to chemotactic stimuli

FATED
course Facies
cold, non-inflamed staph Abscesses
retained primary Teeth
increased IgE
Dermatologic problems (eczema)

Labs: Increased IgE
Chronic mucocutaneous candidiasis
T-cell dysfunction

Candida albicans infxns of skin and mucous membranes.
SCID
Several types --> B and T-cell deficiency
Defective IL-2 receptor (most common, X-linked)
Adenosine deaminase deficiency
Failure to synthesize MHC II Ag

Recurrent viral, bacterial, fungal and protozoal infxns

Tx: Bone marrow transplant (no allograft rejection)
Ataxia-telangiectasia
Defect in DNA repair enzymes

Triad:
cerebellar defects (ataxia)
spider angiomas (telangiectasia)
IgA deficiency
Wiskott-Aldrich syndrome
X-linked recessive defect.
Progressive deletion of B and T-cells.

Triad - TIE:
Thrombocytopenic purpura
Infections
Eczema

Labs: Decreased IgM
Leukocyte adhesion deficiency (type I)
Defect in LFA-1 integrin (CD18) protein on phagocytes

Recurrent bacterial infxns
Absent pus formation
Delayed separation of umbilicus

Labs: Neutrophilia
Chediak-Higashi syndrome
AR inheritance
Defect in microtubular function with decreased phagocytosis

Recurrent pyogenic infxns
Staph and strep
Partial albinism
Peripheral neuropathy
Origin of Systolic murmur that Increases in intensity with Squatting to Standing (rapidly for 30 sec)
Hypertrophic cardiomyopathy
Syngeneic graft
From identical twin or clone.
Allograft
From non-identical individual of same species.
Xenograft
From different species
Hyperacute rejection
Ab mediated (type II)
Preformed anti-donor Abs in recipient

Occurs in minutes after transplantation
Acute rejection
Cel mediated - cytotoxic T-cells against foreign MHCs

Weeks after transplantation.
Reversible with cyclosporin and OKT3
Chronic rejection
T-cell and Ab mediated vascular damage (obliterative vascular fibrosis)

Occurs months to years after transplantation.
Irreversible.
CTL perceives as Class I-MHCself presenting non-self antigen.
GVHD
Grafted T-cells proliferate in irradiated ICH and rejects cells with foreign proteins

Severe organ dysfunction.
Maculopapular rash, jaundice, hepatosplenomegaly, diarrhea
Cyclosporine
Calcineurin inhibitor --> prevents IL-2 and receptor production. Block differentiation and activation of T-cells

Use: Transplant, AI disorders

Toxicity:
Viral Infxns
Lymphoma
Nephrotoxic (prevent with mannitol diuresis)
Tacrolimus
Similar to cyclosporine. Binds FK-binding protein --> Inhibits IL-2 and other cytokine secretion.

Use: Potent, used in transplant

Toxicity: Significant
Nephrotoxicity
Peripheral Neuropathy
HTN
Pleural effusion
Hyperglycemia
Azathioprine
Antimetabolite precursor of 6-MP.
Interferes with metabolism/synthesis of nucleic acids.
Toxic to proliferating lymphocytes.

Use: Kidney transplant, AI disorders (glomerulonephritis, hemolytic anemia)

Toxicity:
BM suppression
Toxic effects of increased allopurinol
OKT3 (muromonab-CD3)
Monoclonal Ab that binds CD3 on T-cell surface
Blocks T-cell signal transduction.

Use: kidney transplant

Toxicity:
Cytokine release syndrome
Hypersensitivity rxn
Sirolimus / Rapamycin
Binds to mTOR.
Inhibits T-cell proliferation in response to IL-2

Use: Kidney transplant
used in combo with cyclosporine and corticosteroids

Toxicity: Hyperlipidemia, Thrombocytopenia, Leukopenia
Mycophenolate mofetil (CellCept)
Inhibits de novo guanine synthesis and block lymphocyte production
Daclizumab
Monoclonal ab with high affinity for IL-2 receptor on activated T-cells
Aldesleukin (IL-2)
Recombinant cytokine

RCC, metastatic melanoma
Erythropoietin (epoetin)
Anemias (esp. in renal failure)
Filgrastim (G-CSF)
Recovery of bone marrow
Sargramostim (GM-CSF)
Recovery of bone marrow
Alpha interferon
Hep B, C
Kaposi sarcoma
Leukemias
Malignant melanoma
Beta interferon
MS
Gamma interferon
CGD
Oprelvekin (IL-11)
Thrombocytopenia
Thrombopoietin
Thrombocytopenia