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Immunology Flashcards

1
Q

what are lymph nodes?

A

1) Act with filtration of B or T cells

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2
Q

What are the parts of the lymph node, and what is the use?

A

1) Follicule: B cell localization
2) Medulla: Drain lymphatics and contain reticular cells
3) Paracortex:houses T cells ( not well developped in DiGeorge syndrome)

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3
Q 
Which part of the body do the following lymph nodes drain? 
Cervical
Hilar
Mediastinal 
Axillary
Celiac
Superior mesenteric
Inferior mesenteric
Internal iliac
Para-aortic
Superficial inguinal 
Popliteal.
A

1) Cervical (head and neck)
2) Hilar (lungs)
3) Mediastinal (Trachea and esophagus)
4) Axillary: Upper limb, breast, skin, ombilical
5) Celiac: liver, stomach, spleen, pancrease
6) Superior mesenteric: lower duodenum, jejunum, ileum, colon to splenic flexure
7) Inferior mesenteric: colon from splenic flexure to upper rectum
8) Internal iliac: lower rectum to anal canal, vagina, cervix, prostate
9) Para-aortic: testes, ovaries, kidnies, uterus
10) Superficial inguinal: anal canal, skin below ombilicus, scrotum,vulva
11) Popliteal: dorsolateral foot, posterior calf

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4
Q

where are T cells found within the spleen?

A

1) Periarteriolar lymphatic sheath

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5
Q

Where are B cells found?

A

In the follicles in the white pulp

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6
Q

What is found in the marginal zones between the red pulp and the white pulp?

A

Macrophages
Specailized B cells
Antigen presenting cells

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7
Q

What is seen in blood smear after a splenectomy?

A

1) Howell-Jolly bodies (nuclear remnants)
2) Target Cells
3) Thrombocytosis: loss of sequestration and removal
4) Lymphocytosis: loss of sequestation

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8
Q

What is the thymus used for?

What are changes to thymus depending on the condition?

A

1) Site of T Cell differentiation and maturation
2) Hypoplastic with DiGeorge’s syndrome
3) Enlarged if have myasthenia gravis.

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9
Q

What are components of inate vs adaptive immunity?

A

1) Inate have neutrophils, macrophages, and noncytes

2) Adpative have: T cells, B cells and antibodies

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10
Q

What is the resistance between inate and adaptive immunity?

A

1) Inate: perists through generations, and does not change within an organismes lifetime
2) Microbial resistance, not heritable

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11
Q

Response to pathogents (inante vs adaptive)

A

1) Inate: rapid

2) Adpative: highly specific, and refined over time, the memory response is faster

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12
Q

What are proteins associated with the rapid/inate?

A

1) Inate: C-reative protein

2) Adaptive: immunoglobulins

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13
Q

How does recognition occur? (Innate vs adaptive)

A

1) Inate: Tollike recpetors
2) Pattern recognition receptors (LPS for gram - bacteria)

3) Adpative: Memory activated B and T cells.

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14
Q

MHC 1 vs MHC 2 in terms of loci?

A

HLA-A, HLA-B, HLA-C (1 letter)

MHC-2 (HLA-DP, HLA-DQ, HLA-DR) (has 2 letters)

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15
Q

MHC 1 vs MHC 2, binding?

A

1) TCR and CD8 (MHC 1)

2) TCR and CD4 (MHC 2)

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16
Q

MHC 1 vs MHC 2 expression?

A

1) MHC1: on all nucleated cells (but not RBC)

2) MHC 2: On all APC

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17
Q

Function of MCH 1 vs MHC 2?

A

MHC 1: endogenously synthesized antigens

MHC 2: Presents exogensously sythesized antigens

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18
Q

What are associated proteins with MHC 1 and MHC 2?

A

B2-microglobulin

Invariant chain

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19
Q 
What are HLA subtypes associated with disease?
Hemochromatosis
B8
B27
DQ2/DQ8
DR2
DR3
DR4
DR5
A

A3: Hemochromatosis
B8: Addison diseasse, mysanthia gravis
B27: PSoratic arthritis, ankylosing spondylitis
DQ2/DQ8: Celiac disease
DR2: Multiple scleosis
DR4: Rheumatoid arthritis. DM
DR5: pernicious anemia (Hashimoto thyroiditis)

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20
Q

What do natural killer cells do?

A

1) Use perforin and granzymes to induce apoptosis of infected cells and tumor cells
2) Activity enhanced by IL 2, Il-12, IFN- alpha

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21
Q

What are the positive and negative selection of T cells?

A

Positive selection: Thymic cortex, capable of binding to self MHC are allowed to survive

Negative selection: Thymic medulla. T cells with high affinity for self antigens undergo apoptosis.

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22
Q

What do helper T cells do?

A

1) TH 1 cell Secrete IFN-Gamma that activate the macs and cytotoxic T cells.
2) Th2 cells: Il-4 and IL-5 (recruits eospinophils for parasitic defense and promote IgE

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23
Q

What is naive T-Cell activation?

A

Dendritic cells do the recognizing

1) Presented to MHC II (either CD4+ or CD8+)
2) Proliferation and survival
3) Cell activates cytokines and kills virus infected cells

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24
Q

What is B cell activation class, switching?

A

1) B cell receptor mediated endocytosis (presented on MHC II)
2) Cell secretes cytokines that Ig Class switch of B cell, and activates the antibody production.

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25
Q

What are the structures of antibody Fab, and the Fc?

A

1) FaB: fragment antigen binding (determines idiotype), only 1 antigenic specificity per B cell
2) Fc (Constant): Carboxyl terminal

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26
Q

How is generation of antibody diversity accomplished?

A

1) Recombination of light and heavy chains
2) Random addition of nucleotides in the chains
3) Recombination of light and heavy chain genes

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27
Q

What immunoglobulin isotypes?

A

1) IgG: delayed response to bacterial toxins and viruses
2) IgA: prevents attachements of bacteria and virus to mucous membrane (secretory)
3) IgM: intermediate response to antigen
4) IgD: Unclear
5) IgE: immnuity to worms by activating eosinophils.

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28
Q

What are the thymus-independent antigens?

A

1) Weakly immunogenic (requires boosters)
2) Thymus dependent: Contain diphtheria vaccins (immnuological memory occur as a result of direct contact with B cells and Th-Cells

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29
Q

What are acute phase reactants?

A

Factors whose serum concentration change significantly in response to inflammation (notably IL-6)

C-reative protein
Ferritin
Fibrinogen
Hepcidin
Serum Amyloid A
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30
Q

What are negative (downregulated) during stress?

A

1) Albumin

2) Transferrin

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31
Q

What does C-reactive protein measure?

A

Facilitates phagocytosis, sign of ongoing inflammation

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32
Q

What does ferritin measure?

A

Binds and sequesters iron to inhibit microbial iron scavenging

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33
Q

What does fibrinogen measure?

A

1) Coagulation factor, promotes endothelial repair (goes with ESR)

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34
Q

What does Hepcidin show?

A

1) Decrease iron absorption, and decrease iron release

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35
Q

What does serum amyloid A show?

A

1) Prolonged elevation can lead to amyloidosis

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36
Q

What does transferrin show?

A

Internalized by macrophages to sequester

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37
Q

Which organ produces the complement system?

A

Hepatically synthesized plasma proteins that defend against gram - bacteria

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38
Q

How is the complement system mediated?

A

By IgG of IgM

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39
Q

What are the functions of complement pathway?

A

C3b opsonization
C3a, C4a, C5a anaphylaxis
C5: neutrophil chemotaxis.

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40
Q

Disorder associated with C1 esterase inhibitor deficiency?

A

1) Angioedmea (unregulated kallikrein, increased bradykinin)

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41
Q

Disorder associated with C3 deficiency?

A

Recurrent sinus and respiratory infection

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42
Q

Disroder associated with C5-C9 deficiency?

A

Increased susceptibility to Neisseria bacteremia

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43
Q

Disorder associated with DAF (GP1-anchored enzyme deficiency)?

A

Complement mediated lysis of RBC

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44
Q

Passive vs active immunity due to acquisition?

A

1) Receiving preformed antibodies vs exposure to foreign antigens

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45
Q

Passivevs active immunity due to onset?

A

Passive is rapid, and active is long lasting protection with memory

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46
Q

Passive vs active immunity duration?

A

Passive: short life span
Active: long lasting (protection)

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47
Q

Examples of passive vs active immunity?

A

IgA in breast milk
IgG crossing placenta

Active: natural infection

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48
Q

What are some examples of passive immunity vaccines?

A

1) Tetanus
2) Botulism
3) HBV
4) Varicella
5) Rabies

When there is exposure to one of these entities, then the vaccine is given, and because works rapidly, can heal.

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49
Q

Which response is activated by the live attenuated vaccine?

A

Cellular and humoral response

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50
Q

what are the pros and cons of live attenuated vaccine?

A

1) Induces lifelong immunity

2) cons: may revert to virulent form *cannot be given if immunocrompromised, or pregnent

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51
Q

What are some examples of live attenuated virus?

A

1) Influenzae
2) Measels
3) BCG
4) Polio (sabine)
5) Varicella
6) yellow fever

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52
Q

What are pros and cons of inactivated or killed vaccine?

A

Pro: safer then live vaccine
Cons: weaker, immune response, and needs a booster

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53
Q

What are the 5 types of hypersensitivity reactions?

A

1) Type 1 (anaphylactic and free antigen crosslinked IgE
(rapid reaction, because has preformed antibodies)

Test with IgE

2) Type 2 Cytotoxic (direct and indirect coombs test)
Direct: detects antibodies bound to patient’s RBC

Indirect: detects serum antibodies

IgM and IgG

3) Type 3: immune complex immune complex-antigen/antibody, its IgG

(Vasculitis or systemic manifestations)

Examples: SLE, polyarertis nodosa, post streptococcal glomerulonephrtis

4) Type 4:Sensitized T cells encounter antigen and the release cytokines (lead to macrophage activation)

Usually this is delayed or last cell mediated, and not transferred by serum.

Examples: Contact dermatitis
Graft vs host disease
Multiple sclerosis

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54
Q

What is serum sickness?

A

Immune complex disease in which antibodies to foreign proteins are produced

might be deposited on membrane and can fix tissue

Can lead to arthus reaction

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55
Q

What are the causes if serum sickness?

A

Drugs acting as haptens

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56
Q

What are the symptoms of serum sickness?

A

1) Fever
2) Urticaria
3) Arthralgia
4) Proteunuria
5) Lymphadenopathy (5-10 days) after antigen exposure

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57
Q

What is Arthrus reaction?

A

1) Antibody medited hypersensitivity reaction
2) Intradermal injection of antigen into pre-senstized skin
3) Have immune complex on the skin leading to edema, necrosis, and activation of the complement

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58
Q

What are possible types of blood transfusion reactions?

A

1) Allergic Reaction
2) Anaphylactic reaction
3) Febrile nonhemolytic transfusion reaction
4) Acute hemolytic transfusion reaction

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59
Q

What is presentation and cause of allergic reaction to blood?

A

1) Hypersensitivity to plasma proteins: urticaria, pruritis, wheezing, fever

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60
Q

Presentation and cause of anaphylactic reaction?

A

IgA deficient individual
Needs to recieve blood products without IgA
Dyspnea, brochospasm, hypotension

Treatment: epinephrine

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61
Q

Presentation and cause of febrile, non hemolytic transfusion reaction?

A

Type 2 hypersensitivty reaction
Host antibodies against donor HLA

Fever
Headaches
Chills
Flushing

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62
Q

Causes and presentation of acute hemolytic transfusion reaction?

A

Type II reaction
Intravascular hemolysis
ABO incompatibility

Fever
Hypotension
Tachycardia 
Flank pain
Hemoglobinuria 
Jaunedice
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63
Q

Autoantibody with anti-ach?

A

Mysanthia gravis

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64
Q

Autoantibody with anti-basement membrane?

A

Goodpasture syndrome

65
Q

Autoanotbody with anticardiolipin, lupus anticoagulant?

A

SLE, Antiphospholipid syndrome

66
Q

Autodantibody with anti-centromere?

A

Limited scleroderma (CREST)

67
Q

Autoantibody with anti desmosome?

A

Pemphigus vulgaris

68
Q

Autoantibody with anti-dsDNA, anti-Smith?

A

SLE

69
Q

Autoantibody with anti-glutamic acid and decarboxylase?

A

Type 1 DM

70
Q

Antihemidesmosome?

A

Bullos pemphigoid

71
Q

Anti-histone?

A

Drug induces lupus

72
Q

Anti-Jo-1, anti-SRP, Anti-Mi 2?

A

Polymyositis, dermatomyositis

73
Q

Antimicrosmal, and antithyroglobulin?

A

Hashimoto thyroiditis

74
Q

Antimitochondrial?

A

Biliary cirrhosis

75
Q

Anti-nuclear (ANA)?

A

SLE (non-specific)

76
Q

Anti-parietal cell?

A

Pernacious anemia

77
Q

Antiphospholipase A 2 receptor?

A

Membraneous nephropathy

78
Q

Anti-Scl-70?

A

Scleroderma diffuse

79
Q

Anti-smooth muscle?

A

Autoimmune hepatitis type 1

80
Q

Anti SS, anti SSB?

A

Sjogen syndrome

81
Q

Anti TSH receptor?

A

Graves disease

82
Q

Anti-U1 RNP?

A

Mixed connective tissue disease

83
Q

Voltage gated calcium channel antibodies?

A

Lambert-eaton

84
Q

Anti-endomysial, IgA anti-tissue transglutaminase?

A

Celiac disease

85
Q

p-ANCA?

A

1) Eosinophilic granulomatosis with polyangitis

Churg-Strauss

86
Q

C-ANCA?

A

Granulomatosis with polyangiitis (Wegener)

87
Q

Rheumatoid factor (IgM antibody that targets IgG Fc)

A

Rheumatoid arthritis

88
Q

Defect, presentation, and findings of X-linked Bruton agammaglobinemia?

A

1) NO B cell maturation
Recurrent bacterial and enteroviral infection
2) Absent B cells in peripheral blood smear
3) Absent lymph nodes and tonsils

89
Q

Defect, presentation, findings selective IgA deficiency?

A

1) Very common
2) Usaully assymptomatic (have airway and GI infections), Autoimmune, atropy anaphylaxis
3) Decreased IgA, normal IgG, and IgM

90
Q

Defect, presentation, findings associated with common variable deficiency?

A

1) Defect in B cell differentiation
2) Can be acquired in the 20-30
3) Increased risk of brochiectasis and lymphoma, and sinus pulmonary infections
4) Decreased plasma cells and decreasedimmunoglobulins

91
Q

What is the complement system?

A

Classic system that is IgG or OgM mediated

92
Q

What are the functions of opsonins?

A

Bacterial defense, to help with phagocytosis

93
Q

What is C1 esterase inhibitor deficiency?

A

Hereditary angioedema due to activation of kallikrien (ACE contrindicated)

94
Q

What is C3 deficiency?

A

1) Increase recurrent pyogenic sinus infections

2) Increase hypersensitivity III reactions

95
Q

What are C3-C9 deficiencies?

A

Susceptibility to recurrent Neisseria bacteria

96
Q

What are DAF (GP1 anchored enzyme) deficiency?

A

Linked to paraoxymal nocturnal hemoglobinuria

97
Q

Why is IL-1 important?

A

Fever

98
Q

IL-2 linked?

A

Stimulates T cells

99
Q

IL-3 linked to?

A

Stimulates bone marrow

100
Q

IL-4 linked to?

A

Stimulare IgE

101
Q

IL-6 linked to?

A

Fever and acute phase proteins

102
Q

TNF-alpha linked to?

A

Mediates septic shock

Cachexia in malignancy

103
Q

what are T-Cells?

A

TCR binds to antigen MHC complex
CD3 (Associated with signal transaction)
CXCR4/CCR5: co receptors for HIV

104
Q

What are B cells associated with?

A

Ig (binds antigen)
CD 19, CD 20
Targets Epstein Barr

105
Q

What are the hematopoietic stem cells associated with?

A

CD 34

106
Q

What is anergy?

A

When a cell is not activated by exposure to antigen
(exposure without the costimulatory signal)
Mechanism of self tolerance

107
Q

What are the effects of bacterial toxins?

A

Staph aureus and pyrogens activate CD 4+ and cause massive release of cytokins

108
Q

How do endotoxins work?

A

Directly stimulare MACS by binding with endotoxin receptor TLR4/CD14

109
Q

What are examples of antigenic variation?

A

1) Can be rearrangement of RNA segments

2) Classic examples include: Salmonella, Borrelia recurrentis, N. Gonorrhea, parasites.

110
Q

Defect, presentation, findings Thymic aplasia?

A

1) 22q11 deletion
2) Failure to develop 3rd and 4th pharyngeal pouches (no thymus or parathyroids)

Presentation: Tetany, controncal Tetralogy of Fallot)

111
Q

Defect, presentation, findings of Il-12 deficiency?

A

1) Decreased Th1 response
2) Mycrobial and fungal infections
3) Present after BCG

112
Q

Defect, presentation, hyper IgE syndrome (Jobs syndrome) ?

A

1) Deficiciency of Th17 cells
2) Impaired of recruitement neutrophils
3) Coarse farcies, staph abcess, retained primary teeth, dermatological problems

113
Q

Defect, presentation, findings, Chronic mucocutaneous candidasis?

A

1) T-Cell dysfunction
2) Non-invasive candida albicans
3) Absent T cell proliferation

114
Q

Defect, presentation, findings with severe combined immunodeficiency?

A

1) Il-2R gamma chain mutation
2) Failure to thrive, diarrhea, thrush, recurrent viral, bacterial, fungal infections
3) Treatment: bone marrow transplant
4) No thymic shadow on x-ray,

115
Q

Defect, presentation, findings of ataxia telangiectasia?

A

1) Defect in ATM gene (can’t repair DNA)
2) Triad of cerebeller defects, ataxia, spider angiomas, IgA deficiency
3) Findings: decreased IgA, IgG, IgE

116
Q

Defect, finding, presentation of Hyper IgM?

A

1) CD40L on Th cell
2) x-linked recessive
3) Severe pyogenic infections
4) pneumocytis cryptosporidium
5) Decreased IgG, IgA, IgE

117
Q

Defect, presentation, findings with Wiskott-aldrich syndrome?

A

1) Mutation in WAS gene

2) Thrombocytopenia, Eczema, recurrent infections,

118
Q

What are leukocyte adhesion deficiency?

A

1) LFA-1 integrin

2) Bacterial skin infection, no pus formation, delayed ombilical cord seperation

119
Q

Defect, presentation, findings Chdiak-Higashi syndrome?

A

1) Defect in LYST gene
2) Recurrent pyogenic infections by staph
3) Peripheral neuropathy, neurodegeneration
4) Pancytopenia, and coagulation defects

120
Q

Defect, presentation, findings of chronic granulomatous disease?

A

1) Defect in NAPH oxidase (X-linked)
2) Increased susceptibility to catalase organisms (Nocardia, Pseudomonas, Listeria)
3) Findings: abnormal dihydrorhadamine

121
Q

What are common bacterial infections associated with immunodeficiency?

A

1) Pseudonomas aeruginosa
2) Strep pneumoniae
3) H. Influenzae
4) N. Meningitidis
5) E. Coli
6) Klebsiella pneumoniae

122
Q

Common virus infection of immunodeficiency?

A

1) CMV
2) EBV
3) VZV
4) Enteroviral encephalitis

123
Q

Common fungi and parasite infections in immunodeficiency?

A

Candida (aspergillus systemic)

Giardiasis

124
Q

What are the types of grafts?

A

1) Auto grafts (from self)
2) Syngeneic graft (from identical twin or clone)
3) Allograft: nonidentical individual of the same species
4) Xenografts: from different species

125
Q

Onset, pathogenesis, features of hyperacute reaction?

A

1) Onset within minutes
2) Pre-existing antibodies react with donor antigen
3) Hypersensitivity reaction
4) Widespread thromosis of graft vessels with ischemia and necrosis (need to remove the graft)

126
Q

Onset, pathogenesis, features of acute infection?

A

1) Weeks to months
2) CD8 + cells are activated against the MHC (similar to hyperacute, except the antibodies develop after transplant)
3) Vasculitis with dense interstitial lymphocyte
4) Prevent, reverse with immunosuppression

127
Q

Onset, pathogenesis, features of chronic infection?

A

1) Months to years
2) CD4+ cells respond to APC (Both cellular and humoral reaction)
3) Recipient secrete cytokines, proliferation of vascular smooth muscles
4) Brpnchiolitis obliterans, accelerated atherosclerosis, chronic graft nephropathy, vanishing bile duct

128
Q

Onset, pathogenesis, features of graft-vs. host disease?

A

1) Grafted immunocompetent T cells proliferate, and reject host cells as foreign
2) Severe organ dysfunction
3) Type of IV hypersensitivity reaction
4) Maculopapular rash, jaunedice, diarreha, hepatosplenomegaly

Usually in bone marrow and lvier transplant

Can be beneficial in bone marrow transplant (the graft attacks the tumor)

129
Q

Mechanism, Use, toxicity of cyclosporin?

A

1) Calcineurin inhibitor (prevent IL-2 transcription)
2) Used in transplant, psoraisis, rheumatoid arthritis
3) Nephotoxic, HTN, neurotoxicity, gingival hyperplasia

130
Q

Mechanism, use, toxicity, tacrolimus (FK506)?

A

1) Calcinurin (prevent IL-2 transcription)
2) Transplant rejection
3) Nephrotoxicity, diabtetes, hirutism

131
Q

Mechanism, use, toxicity sirolimus?

A

1) mTOR inhibitor, prevents IL-2
2) Kidney transplant
3) Pancytopenia, insulin resistance, hyperlipidemia (NOY nephrotoxicity)

132
Q

Mechanism, Use, toxicity daclizumab, basilixmab?

A

1) Blocks IL-2
2) Used in kidney transplant
3) HTN, tremor

133
Q

Mechanism, use, toxicity, azathioprine?

A

1) Anti-metabolite (inhibit lymphocyte proliferation)
2) Transplant rejection, rheumatoid arthritis, Crohn, glomerulonephritis
3) Leukopenia, anemia, thrombocytopenia

134
Q

Mechanism, use,toxicity of MMF?

A

1) Prevents purine synthesis of B and T cells
2) Transplant rejection, rheumatoid arthritis, lupus nephritis
3) GI upset, pancytopenia, HTN, hyperglycemia, less neurotoxic and nephrotoxic

135
Q

Mechanism, use, toxicity of corticosteroids?

A

1) Suppress B and T cells, induce apoptosis of T lymphoctyes
2) Transplant rejection and prophylaxis, autoimmune and inflammatory disorders
3) Hyperglycemia, osteoporosis, central obesity, avascular necrosis of femoral head, psychosis

136
Q

Adesleukin IL-2 (recombinent cytokines) agent and clinical uses?

A

1) Renal cell carcinoma, and metastatic melanoma

137
Q

Recombinent cytokines Epoetin alfa?

A

Anemias

138
Q

Filgrastin (G-CSF)?

A

Recovery for bone marrow

139
Q

Sargramostim (GM-CSF)?

A

Recovery of bone marrow

140
Q

IFN-alpha?

A

1) Chronic hepatitis B and C, Kaposi Sarcoma, malignant melanoma

141
Q

IFN- Beta?

A

1) Multiple sclerosis

142
Q

IFN-gamma?

A

Chronic granulomatous disease

143
Q

Romiplostin, eltrombopage (Thrombopoietin receptor agonist)?

A

Thrombocytopenia

144
Q

Oprelvekin?

A

Thrombocytopenia

145
Q

Cancer therapy: Alemtuzumab?

A

1) Target: CD52

2) Clinical use: CLL, MS

146
Q

Cancer therapy Bevacizumab?

A

1) Target VEGF

2) colorectal cancer, renal cell carcinoma

147
Q

Cancer therapy Cetuximab?

A

1) Target EGFR
2) Stage IV colorectal cancer
3) Head and neck cancer

148
Q

Cancer therapy Rituximab?

A

1) Targets CD 20
2) B Cell, non-hodgkin
3) Lymphoma

149
Q

Cancer therapy Trastuzumab?

A

1) Her2/neu

2) Breast cancer

150
Q

What are threee medications that can be used to treat IBD, rheumatoid arthritis, ankolizing spondylitis and psorarias?

A

1) Adalimumab, certolizumab, infliximab

2) Works on soluable TNF-alpha

151
Q

Autoimmune therapy eculizumab?

A

1) Complement protein C5

2) Paroxysmal nocturnal hemoglobinuria

152
Q

Autoimmune therapy natalizumab?

A

1) Alpha 4 integrin
2) Multiple sclerosis
3) Crohn’s disease

153
Q

What are other applications for abciximab?

A

1) Platelet glycoprotiens IIb/IIIA

2) Antiplatelet for prevention of ischemic complications in patients

154
Q

What are other uses for denosumab?

A

1) Osteoporosis (inhibits osteoclasts)

155
Q

What are applications for digoxin Fab?

A

1) Antidote for digoxin toxicity

156
Q

Applications for omalizumab?

A

1) Targets IgE

2) Prevents allergic asthma

157
Q

Applications for Palizumab?

A

1) RSV F protein

2) RSV prophylaxis for high risk infants

158
Q

What medication can be used for age related macular degeneration?

A

1) Ranibizumab

2) Bevacizumab

US (17 decks)

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