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Immunology Flashcards

1
Q

Lymph node

A

A secondary lymphoid organ that has many afferents, 1 or more efferents. Encapsulated, with trabeculae. Functions are nonspecific filtration by macrophages, storage of B and T cells, and immune response activation.

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2
Q

Follicles of lymph nodes

A

Site of B-cell localization and proliferation. In outer cortex. Primary follicles are dense and dormant. Secondary follicles have pale central germinal centers and are active.

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3
Q

Medulla of lymph nodes

A

Consists of medullary cords (closely packed lymphocytes and plasma cells) and medullary sinuseses. Medullary sinuses communicate with efferent lymphatics and contain reticular cells and macrophages.

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4
Q

Paracortex of lymph nodes

A

Houses T cells. Region of cortex between follicles and medulla. Contains high endothelial venules through which T and B cells enter from blood. Not well developed in patients with DiGeorge syndrome. Paracortex enlarges in an extreme cellular immune response (eg viral infection).

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5
Q

Lymph drainage of head and neck

A

cervical lymph node

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6
Q

Lymph drainage of lungs

A

hilar lymph node

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7
Q

Lymph drainage of trachea and esophagus

A

mediastinal lymph nodes

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8
Q

Lymph drainage of upper limb, breast, skin above umbilicus

A

Axillary lymph nodes

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9
Q

Lymph drainage of liver, stomach, spleen, pancreas, and upper duodenum

A

celiac lymph nodes

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10
Q

Lymph drainage of lower duodenum, jejunum, ileum, colon to splenic flexure

A

superior mesenteric lymph nodes

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11
Q

Lymph drainage of colon from splenic flexure to upper rectum

A

inferior mesenteric lymph nodes

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12
Q

Lymph drainage of lower rectum to anal canal (above pectinate line), bladder, vagina (middle third), prostate

A

internal iliac lymph nodes

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13
Q

Lymph drainage of testes, ovaries, kidneys, uterus

A

para-aortic lymph nodes

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14
Q

Lymph drainage of anal canal (below pectinate line), skin below umbilicus (except popliteal territory), scrotum

A

superficial inguinal lymph nodes

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15
Q

Lymph drainage of dorsolateral foot and posterior calf

A

popliteal lymph nodes

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16
Q

right lymphatic duct

A

drains right side of body above the diaphragm

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17
Q

thoracic duct

A

drains everything but the right side of body above the diaphragm

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18
Q

Sinusoids of spleen

A

Long, vascular channels in red pulp with fenestrated “barrel hoop” basement membrane. T cells are found in the periarteriolar lymphatic sheath (PALS) within the white pulp of the spleen. B cells are found in follicles within the white pulp of the spleen. The marginal zone, in between the red pulp and white pulp, contains APCs and specialized B cells, and is where APCs capture blood-borne antigens for recognition by lymphocytes. Red pulp is found peripherally, and the white pulp is found centrally. Macrophages found nearby in spleen remove encapsulated bacteria.

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19
Q

Splenic dysfunction (eg postsplenectomy, sickle cell disease)

A

a decrease in IgM leads to a decrease in complement activation causing a decrease in C3b opsonization and creating an increase susceptibility to encapsulated organisms. Common infections include (SHiNE SKiS): Streptococcus pneumoniae, Haemophilus influenzae type b, Neisseria meningitidis, Escherichia coli, Salmonella spp., Klebsiella pneumoniae, Group B Streptococci.

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20
Q

Postsplenectomy histology

A

Howell-Jolly bodies (nuclear remnants), target cells, thrombocytosis (loss of sequestration and removal), and lymphocytosis (loss of sequestration).

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21
Q

Thymus

A

Site of T cell differentiation and maturation. Encapsulated. THymus is derived from the THird pharyngeal pouch. Lymphocytes of mesenchymal origin. Cortex is dense with immature T cells; medulla is pale with mature T cells and Hassall corpuscles containing epithelial reticular cells. T cells= Thymus. B cells=Bone marrow

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22
Q

Innate immunity

A

Made up of neutrophils, macrophages, monocytes, dendritic cells, natural killer cells (lymphoid origin), complement. It is germline encoded. Resistance to the innate immunity through generations; does not change within an organism’s lifetime. Response to pathogen is non-specific and occurs rapidly (minutes to hours). Physical barriers apart of the innate immunity includes epithelial tight junctions and mucus. Secreted proteins include lysozyme, complement, c-reactive protein (CRP), defensins. Key features in pathogen recognition includes toll-like receptors (TLRs), which are patteren recognition receptors that recognize pathogen-associate molecular patterns (PAMPs). Examples of PAMPs include LPS (gram-negative bacteria), flagellin (bacteria), ssRNA (viruses).

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23
Q

Adaptive immunity

A

Made up of T cells, B cells, and circulating antibodies. It has variation through V(D)J recombination with lymphocyte development. Microbial resistance is not inheritable. Response to pathogens is highly specific and is refined over time. It develops over long periods but memory response is faster and more robust. Immunoglobulins are secreted. Memory cells include activated B and T cells; subsequent exposure to a previously encountered antigen leads to a stronger and quicker immune response.

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24
Q

MHC I and II

A

MHC encoded by HLA genes. Present antigen fragments to T cells and bind T-cell receptors (TCRs).

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25
Q

MHC I

A

Loci include HLA-A, HLA-B, HLA-C. Binds TCR and CD8. It is expressed on all nucleated cells, but are not expressed on RBC’s. They present endogenously synthesized antigens (eg viral or cytosolic proteins) to CD8+ cytotoxic T cells. Antigen peptides are loaded onto MHC I in RER after delivery via TAP (transporter associated with antigen processing). A component of MHC class I molecules is beta2-microglobulin.

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26
Q

MHC II

A

Loci include HLA-DR, HLA-DP, HLA-DQ. Binds to TCR and CD4. They are expressed on APCs. They present exogenously synthesized antigens (eg bacterial proteins) to CD4+ helper T cells. Antigens are loaded following release of invariant chain in an acidified endosome. A polypeptide involved in the formation and transport of MHC class II protein is invariant chain.

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27
Q

HLA-A3

A

Associated with hemochromatosis.

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28
Q

HLA-B27

A

Associated with Psoriatic arthritis, Ankylosing spondylitis, arthritis of Inflammatory bowel disease, Reactive arthritis (formerly Reiter syndrome). (PAIR). Also known as seronegative arthropathies.

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29
Q

HLA-DQ2/DQ8

A

Associated with celiac disease

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30
Q

HLA-DR3

A

associated with diabetes mellitus type 1, SLE, Graves disease, Hashimoto thyroiditis.

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31
Q

HLA-DR2

A

Multiple sclerosis, hay fever, SLE, Goodpasture syndrome

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32
Q

HLA-DR4

A

Rheumatoid arthritis, diabetes mellitus type 1. There are 4 walls to a “rheum”

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33
Q

HLA-DR5

A

Associated with pernicious anemia, which leads to vitamin B12 deficiency and Hashiomoto thyroiditis.

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34
Q

Natural killer cells

A

Use perforin and granzymes to induce apoptosis of virally infected cells and tumor cells. They are lymphocyte members of innate immunity. Their activity is inhanced by IL-2, IL-12, IL-alpha, and IL-beta. They are induced to kill when exposed to a nonspecific activation signal on target cell and/or to an absence of class I MHC on target cell surface. Also kills via antibody-dependent cell-mediated cytotoxicity (CD16 binds Fc region of bound Ig, activating the NK cell).

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35
Q

B-cell functions

A

They recognize antigens and undergo somatic hypermutation to optimize antigen specificity. They also produce antibodies and differentiate into plasma cells to secrete specific immunoglobulins. They also maintain immunologic memory. Memory B cells persist and accelerate future response to antigen.

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36
Q

T-cell functions

A

CD4+ T cells help B cells make antibodies and produce cytokines to recruit phagocytes and activate other leukocytes. CD8+ T cells directly kill virus-infected cells. Delayed cell-mediated hypersensitivity (type IV). Acute and chronic cellular organ rejection. Rule of 8: MHC II X CD4=8; MHC 1 X CD8=8.

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37
Q

Differentiation to Th1 cell from helper T cells

A

requires IL-12

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38
Q

Differentiation to Th2 cell from helper T cells

A

requires IL-4

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39
Q

Differentiation to Th17 cell from helper T cells

A

TGF-beta and IL-6

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40
Q

Th1 cell

A

A helper T cell. Secrete IFN-gamma. Activates macrophages and cytotoxic T cells. They are activated by INF-gamma and IL-12. They inhibited by IL-4 and IL-10 (from Th2 cells). Macrophages release IL-12, which stimulates T cells to differentiate into Th1 cells. Th1 cells release IFN-gamma to stimulate macrophages. Helper T cells have CD4, which binds to MHC II on APCs.

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41
Q

Th2 cell

A

Secretes IL-4, IL-5, IL-10, and IL-13. They recruit eosinophil for parasite defense and promotes IgE production by B cells. They are activated by IL-4. They are inhibited by IFN-gamma (from Th1 cell).

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42
Q

Cytotoxic T cells

A

They kill virus-infected, neoplastic, and donor graft cells by inducing apoptosis. They release cytotoxic granules containing preformed proteins (eg perforin, granzyme B). Cytotoxic T cells have CD8, which binds to MHC I on virus-infected cells.

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43
Q

Regulatory T cells

A

They help maintain specific immune tolerance by suppressing CD4 and CD8 T cell effector functions. They are identifiable by expression of CD3, CD4, CD25, and FOXP3. Activated by regulatory T cells produce anti-inflammatory cytokines (eg IL-10, TGF-beta).

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44
Q

T and B cell activation

A

Antigen-presenting cells (APCs) include B cells, macrophages, and dendritic cells. Two singals are required for T-cell activation, B-cell activation, and class switching.

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45
Q

Steps for naive T-cell activation

A
  1. Dendritic cell (specialized APC) samples and processes antigen. 2. Dendritic cell migrates to the draining lymph node. 3. Foreign antigen is presented on MHC II and recognized by TCR on Th (CD4+) cell. Antigen is presented on MHC I to Tc (CD8+) cell. 4. “Costimulatory signal” is given by interaction of B7 and CD28 (signal 2). 5. Th cell activates and produces cytokines. Tc cell activates and is able to recognize and kill virus-infected cell.
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46
Q

Steps B-cell activation and class switching

A
  1. Th-cell activation as above. 2. B-cell receptor- mediated endocytosis; foreign antigen is presented on MHC II and recognized by TCR on Th cell (signal 1). 3. CD40 ligand (CD40L) on Th cell (signal 2). 4. Th cell secretes cytokines that determine Ig class switching B cell. B cell activates and undergoes class switching, affinity maturation, and antibody production.
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47
Q

Antibody structure and function

A

Fab (variable) region consisting of light (L) and heavy (H) chains recognizes antigens. Fc region of IgM and IgG fixes complement. Heavy chain contributes to Fc and Fab regions. Light chain contributes only to Fab region.

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48
Q

Fab region of antibodies

A

Fragment that does the Antigen Binding. Determines idiotype creating a unique antigen-binding pocket; only 1 antigenic specificity expressed per B cell.

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49
Q

Fc region of antibodies

A

This region is constant, with carboxy terminal. It also binds complement. Also has carbohydrate side chains. It determines isotype (IgM, IgD, ect).

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50
Q

Generation of the diverse region in antibodies

A

Random recombination of VJ (light-chain) or V(D)J (heavy chain) genes. Random combination of heavy chains with light chains. Somatic hypermutation (following antigens stimulation). Addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase.

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51
Q

Immunoglobulin isotypes

A

Mature B cells express IgM and IgD on their surfaces. They may differentiate in germinal centers of lymph nodes by isotype switching (gene rearrangement; mediated by cytokines and CD40L) into plasma cells that secrete IgA, IgE, or IgG.

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52
Q

IgG

A

Main antibody in secondary (delayed) response to an antigen. Most abundant isotype in serum. Fixes complement, crosses the placental (provides infants with passive immunity), opsonizes bacteria, neutralizes bacterial toxins and viruses

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53
Q

IgA

A

Prevents attachment of bacteria and viruses to mucous membranes; does not fix complement. Monomer in circulation or dimer when secreted. Crosses epithelial cells by transcytosis. Produced in GI tract (eg by Peyer patches) and protects against gut infections (eg Giardia). Most produced antibody overall, but has a lower serum concentration. Released into secretions (tears, saliva, mucus) and breast milk. Picks up secretory component from epithelial cells before secretion.

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54
Q

IgM

A

Produced in the primary (immediate)response to an antigen. Fixes complement but does not cross the placenta. It also acts as the antigen receptor on the surface of B cells. They are monomers on B cell and pentamers when secreted. The pentamer structure allows for avid binding to an antigen while the humoral response evolves.

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55
Q

IgD

A

It has unclear function. It is found on the surface of many B cells and in the serum.

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56
Q

IgE

A

It binds to mast cells and basophils; it cross-links when exposed to allergen (two IgE binding the same allergen), thereby mediating immediate (type I) hypersensitivity through release of inflammatory mediators such as histamine. Mediates immunity to worms by activating eosinophils. It has the lowest concentration in serum.

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57
Q

Opsonization by antibody

A

Antibody promotes phagocytosis

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58
Q

Neutralization by antibody

A

Antibody prevents bacterial adherence

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59
Q

Complement activation by antibody

A

Activates membrane attack complex (MAC) and C3b, enhancing opsonization and lysis. Complement binding region is the CH2 region of the Fc.

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60
Q

Differentiation of T cells

A

T cells precursors are made in the bone marrow and than move to the thymus (at this point they express CD4+, CD8+, and T-cell receptor, which binds MHC I or MHC II) where they undergo positive and negative selection. By the time the T cell reaches the thymic medulla, it is differentiated. They then travel to the lymph node to wait for activation. Cytotoxic T cells kill virus-infected, neoplastic, and donor graft cells. Helper T cells will further differentiate once activated (eg Th1, Th2, Th17).

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61
Q

Positive selection of T cells

A

Occurs the in the thymic cortex. T cells expressing TCRs (T-cell receptors) are capable of binding surface self MHC molecules survive.

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62
Q

Negative selection of T cells

A

Occurs in the medulla of the thymus. T cells expressing TCRs with high affinity for self antigens undergo apoptosis.

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63
Q

Thymus independent antigens

A

Antigens lack a peptide component (eg lipopolysaccharides from gram negative bacteria). They cannot be presented by MHC to T cells. They are weakly or non-immunogenic. Vaccines often require boosters and adjuvants (eg pneumococcal polysaccharide vaccine).

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64
Q

Thymus dependent antigens

A

Antigens containing a protein component (eg diphtheria vaccine). Class switching and immunologic memory occur as a result of direct contact of B cells with Th cells (CD40-CD40L interaction).

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65
Q

Acute phase reactants

A

Factors whose serum concentrations change significantly in response to inflammation; produced by the liver in both acute and chronic inflammatory states. It is notably induced by IL-6. Up regulated proteins include CRP, ferritin, fibrinogen, hepcidin, and serum amyloid A. Down regulated proteins include albumin and transferrin.

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66
Q

C-reactive protein

A

Up regulated during acute phase reactants. It is an opsonin; it also fixes complement and facilitates phagocytosis. It is measured clinically as a sign of ongoing inflammation.

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67
Q

Ferritin

A

Up regulated during acute phase reactants. It binds and sequesters iron to inhibit microbial iron scavenging.

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68
Q

Fibrinogen

A

Up regulated during acute phase reactants. It is an coagulation factor, promotes endothelial repair, and correlates with ESR.

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69
Q

Hepcidin

A

Up regulated during acute phase reactants. It prevents release of iron bound by ferritin, which is the cause of anemia of chronic disease.

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70
Q

Serum amyloid A

A

Up regulated during acute phase reactants. Prolonged elevation can lead to amyloidosis.

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71
Q

Albumin

A

Down regulated during acute phase reactants. Reduced concentration conserves amino acids for positive reactants.

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72
Q

Transferrin

A

Down regulated during acute phase reactants. It is internalized by macrophages to sequester iron.

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73
Q

Complement system

A

System of hepatically synthesized plasma proteins that play a role in innate immunity and inflammation. Membrane attack complex (MAC) defends against gram-negative bacteria.

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74
Q

Classic complement pathway

A

It is IgG or IgM mediated. (GM makes classic cars)

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75
Q

Alternative complement pathway

A

It is activated by microbe surface molecules.

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76
Q

Lectin pathways

A

It is activated by mannose or other sugars on microbes surface.

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77
Q

C3b

A

responsible for opsonization (b binds bacteria)

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78
Q

C3a

A

responsible for anaphylaxis

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79
Q

C4a

A

responsible for anaphylaxis

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80
Q

C5a

A

responsible for anaphylaxis and neutrophil chemotaxis.

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81
Q

C5b-9

A

It is responsible for attracting MAC leading to cytolysis.

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82
Q

Opsonins

A

C3b and IgG are the two primary opsonins in bacterial defense and enhances phagocytosis. C3b also helps clear immune complexes. Opsonin=to prepare for eating.

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83
Q

Inhibitors of complement system

A

Decay accelerating factor (DAF, aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells (eg red blood cells).

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84
Q

C1 esterase inhibitor deficiency

A

Causes hereditary angioedema. Ace inhibitors are contraindicated.

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85
Q

C3 deficiency

A

Increases risk of severe, recurrent pyogenic sinus and respiratory tract infections; there is an increase susceptibility to type III hypersensitivity reactions.

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86
Q

C5-C9 deficiencies

A

Terminal complement deficiency increases susceptibility to recurrent Neisseria bacteremia.

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87
Q

DAF (GPI-anchored enzyme) deficiency

A

Causes complement- mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria.

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88
Q

Important cytokines

A

Hot T-bone stEAK: IL-1: fever (hot), IL-2: stimulates T cells, IL-3: stimulates bone marrow, IL-4: stimulates IgE production, IL-5: stimulates IgA, IL-6 stimulates aKute-phase protein production.

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89
Q

IL-1

A

Secreted by macrophages. Also called osteoclast-activating factor. It causes fever, acute inflammation. It activates endothelium to express adhesion molecules. Induces chemokine secretion to recruit WBCs.

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90
Q

IL-2

A

It is secreted by all T cells. It stimulates the growth of helper, cytotoxic, and regulatory T cells, and NK cells.

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91
Q

IL-3

A

It is secreted by all T cells. It stimulates growth and differentiation of bone marrow stem cells. It functions like GM-CSF.

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92
Q

IL-4

A

It is secreted from Th2 cells. It induces differentiation into Th2 cells. It promotes the growth of B cells and stimulates IgE and IgG production

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93
Q

IL-5

A

It is secreted from Th2 cells. It promotes the growth of B cells and stimulates IgA production. It also stimulates growth and differentiation of eosinophils.

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94
Q

IL-6

A

Secreted by macrophages. It causes fever and stimulates production of acute phase proteins

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95
Q

IL-8

A

Secreted by macrophages. It is major chemotactic factor for neutrophils

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96
Q

IL-12

A

Secreted by macrophages. It induces differentiation of T cells into Th1 cells and activates NK cells.

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97
Q

TNF-alpha

A

Secreted by macrophages. It mediates septic shock. It activates endothelium. It causes WBC recruitment and vascular leak. It causes cachexia in malignancy.

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98
Q

Interferon-gamma

A

It is secreted from Th1 cells. It is also secreted by NK cells in response to IL-12 from macrophages. It also stimulates macrophages to kill phagocytosed pathogens. It also activates NK cells to kill virus-infected cells. It increases MHC expression and antigen presentation by all cells.

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99
Q

IL-10

A

It is secreted by Th2 cells. It modulates inflammatory response. It also decreases expression of MHC class II and Th1 cytokines (interferon-gamma). It also inhibits activated macrophages and dendritic cells. It is also secreted by regulatory T cells. Both TGF-beta and IL-10 both atTENuate the immune response.

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100
Q

Cytokines secreted by macrophages

A

IL-1, IL-6, IL-8, IL-12, TNF-alpha.

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101
Q

Cytokines secreted by all T cells

A

IL-2 and IL-3

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102
Q

Cytokines secreted by Th1 cells

A

Interferon-gamma

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103
Q

Cytokines secreted by Th2 cells

A

IL-4, IL-5, and IL-10

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104
Q

Respiratory burst (oxidative burst)

A

It involves the activation of the phagocyte NADPH oxidase complex (eg in neutrophils, monocytes), which utilizes O2 as a substrate. It plays an important role in the immune response by causing a rapid release of reactive oxygen species (ROS). NADPH plays a role in both the creation and neutralization of ROS. Myeloperoxidase is a blue-green heme-containing pigment that gives sputum its color. Phagocytes of patients with chronic granulomatous disease can utilize H2O2 generated by invading organisms and convert it to ROS. Patients are at an increase risk for infection by catalase positive species (eg S. aureus, Aspergillus) capable of neutralizing their own H2O2, leaving phagocytes without ROS for fighting infections.

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105
Q

Pyocyanin

A

Produced by P. aeruginosa, functions to generate ROS to kill competing microbes.

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106
Q

Lactoferrin

A

A protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation.

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107
Q

Respiratory burst pathway

A
  1. NADPH oxidase converts O2 into a superoxide anion, creating NADP+ from NADPH in the process (deficiency=chronic granulomatous disease). 2. Superoxide dismutase converts a superoxide anion into H2O2. 3. Myeloperoxidase creates HCLO* from H2O2. These first three steps occur in the phagolysosome. 4. Glutathione peroxidase uses H2O2 to convert glutathione (GSH-an antioxidant) into glutathione disulfide (GSSG). This reaction requires selenium. 5. Glutathione reductase recreates GSH using NADPH (from the HMP shunt). This reaction also requires selenium. 6. G6PD replenishes NADPH using glucose-6-p
108
Q

Interferon alpha and beta

A

Interfere with viruses. They are apart of innate host defense against both RNA and DNA viruses. Interferons are glycoproteins synthesized by virus-infected cells that act locally on uninfected cells, priming them for viral defense by helping to selectively degrade viral nucleic acid and protein. Essentially results in apoptosis, thereby disrupting viral amplification.

109
Q

T cell receptor

A

On all T cells, binds antigen-MHC complex

110
Q

CD3

A

On all T cells, it is associated with TCR for signal transduction.

111
Q

CD28

A

On all T cells, binds B7 on APC.

112
Q

CD4

A

On helper and regulatory T cells

113
Q

CD40L

A

On helper T cells, binds to APC (B cells and macrophages)

114
Q

CD8

A

On cytotoxic T cells.

115
Q

CD25

A

On regulatory T cells

116
Q

CD19

A

On B cells.

117
Q

CD20

A

On B cells.

118
Q

CD21

A

On B cells, the receptor for EBV. You can drink Beer at the (epstein) Barr when you’re 21

119
Q

CD40

A

On B cells and macrophages, binds helper T cells (CD40L).

120
Q

B7

A

On B cells and macrophages, binds CD28 on T cells.

121
Q

CD14

A

On macrophages

122
Q

Fc and C3b receptors

A

On macrophages, enhances phagocytosis.

123
Q

CD16

A

On NK cells, it binds Fc of IgG

124
Q

CD56

A

A unique marker for NK cells.

125
Q

CD34

A

On hematopoietic stem cells

126
Q

Anergy

A

A state during which a cell cannot become activated by exposure to its antigen. T and B cells become anergic when exposed to their antigens without costimulatory signal (signal 2). Another mechanism of self-tolerance.

127
Q

Superantigens

A

Superantigens (S. pyogens and S. aureus) cross-link the beta region of the T-cell receptor to the MHC class II on APCs. Can activate any CD4+ T cell, causing a massive release of cytokine.

128
Q

Endotoxins

A

Lipopolysaccharides are on gram negative bacteria and directly stimulate macrophages by binding to endotoxin receptor TLR4/CD14; Th cells are not involved.

129
Q

Antigenic variation

A

Some mechaisms for variation include DNA rearrangement and RNA segment reassortment (eg influenza major shift). Classic examples from bacteria include Salmonella (2 flagellar variants), N. gonorrhoeae (pilus protein), and Borrelia recurrentis (relapsing fever). Viral examples include influenza, HIV, and HCV. Examples from parasites include trypanosomes.

130
Q

Passive immunity

A

Acquired through receiving preformed antibodies. Onset is rapid. Duration is the life span of antibodies, short (half life of 3 weeks). Examples include IgA in breast milk, maternal IgG crossing placenta, antitoxin, humanized monoclonal antibody. After exposure to Tetanus toxin, Botulinum toxin, HBV, Varicella, or Rabies virus, unvaccinated patients are given preformed antibodies (To Be Healed Very Rapidly)

131
Q

Active immunity

A

Acquired through exposure to foreign antigens. Onset is slow. Results are long lasting protections (memory). Examples include natural infection, vaccines (induces an active immune response, humoral and/or cellular, to specific antigens), and toxoid. Combined passive and active immunizations can be given for hepatitis B or rabies exposure.

132
Q

Live attenuated vaccines

A

Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host. Induces cellular and humoral responses. MMR is the only live attenuated vaccine given to person with HIV. It induces strong, often life long immunity. However, it may revert to virulent form. Often contraindicated in pregnancy and immunodeficiency. Examples include measles, mumps, rubella, polio (Sabin), influenza (intranasal), varicella, and yellow fever.

133
Q

Inactivated or killed vaccine

A

Pathogen is inactivated by heat or chemicals. Maintaining epitope structure on surface antigens is important for immune response. Mainly induces a humoral response. It is safer than live vaccines. However, it confers a weaker immune response; booster shots are usually required. Examples include Rabies, Influenza (infection) Polio (Salk), hepatitis A (R.I.P. Always)

134
Q

Type I hypersensitivity

A

Includes anaphylactic and atopic responses. Free antigen cross-links IgE on presensitized mast cells and basophils, triggering immediate release of vasoactive amines that act at postcapillary venules (i.e. histamine). Reaction develops rapidly after antigen exposure because of preformed antibody. Delayed response follows due to production of arachidonic acid metabolites (eg leukotrienes). First type and Fast. Skin test for specific IgE.

135
Q

Type II hypersensitivity

A

It is cytotoxic (antibody mediated). IgM, IgG bind to fixed antigen on what is presumed an enemy cell, leading to cellular destruction. There are three mechanisms: ospsonization and phagocytosis, complement- and Fc receptor-mediated inflammation, and antibody-mediated cellular dysfunction. Type II is Cy-2-toxic. Antibody and complement lead to MAC. Tests include direct and indirect Coombs tests.

136
Q

Direct Coomb’s test

A

Detects antibodies that have adhered to patient’s RBCs (eg test for an Rh+ infant of an Rh negative mother.

137
Q

Indirect Coomb’s Test

A

Detects serum antibodies that have adhered to other RBCs (eg test an Rh negative woman for Rh positive antibodies).

138
Q

Type III hypersensitivity

A

Mediated by immune complexes. Antigen- antibody (IgG) complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes. In type III reaction, imagine an immune complex as 3 things stuck together: antigen-antibody-complement.

139
Q

Serum sickness

A

A type III hypersensitivity reaction. An immune complex disease in which antibodies to foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes, where they fix complement (leading to tissue damage). More common than Arthus reaction. Most serum sickness is now caused by drugs (not serum) acting as haptens. Fever, urticaria, arthralgia, proteinuria, lymphadenopathy occur 5-10 days after antigen exposure.

140
Q

Arthus reaction

A

A type III hypersensitivity reaction. A local subacute antibody- mediated hypersensitivity reaction. Intradermal injection of antigen induces antibodies, which form antigen-antibody complexes in the skin. Characterized by edema, necrosis, and activation of complement. Antigen-atibody complexes cause the Arthus reaction. Test includes immunofluorescent staining.

141
Q

Type IV hypersensitivity

A

It is a delayed (T-cell) mediated type reaction. Sensitized T cells encounter an antigen and then release cytokines (which leads to macrophage activation; no antibody involved). 4th and last=delayed. Cell mediated and therefore it is not transferable by serum. 4 T’s= T cells, Transplant rejections, TB skin tests, Touching (contact dermatitis). Tests include PPD and patch test.

142
Q

Hypersensitivity types

A

ACIDS: Anaphylactic and Atopic (type I), Cytotoxic (antibody mediated, type II), Immune complex (type III), Delayed (cell mediated, type IV)

143
Q

Examples of type I hypersensitivity disorders

A

Allergic and atopic disorders (eg rhinitis, hay fever, eczema, hives, asthma). Anaphylaxis (eg bee sting, some food/drug allergies). It is immediate, anaphylactic, and atopic.

144
Q

Examples of type II hypersensitivity disorders

A

Acute hemolytic transfusion reactions, autoimmune hemolytic anemia, bullous pemphigoid, erythroblastosis fetalis, goodpasture syndrome, graves disease, guillain barre syndrome, idiopathic thrombocytopenic purpura, mysathenia gravis, pemphigus vulgaris, pernicious anemia, rheumatic fever. Diseases tend to be specific to tissue or site where antigen is found.

145
Q

Examples of type III hypersensitivity disorders

A

Arthus reaction (eg swelling and inflammation following tetanus vaccine), SLE, polyarteritis nodosa, poststreptococcal glomerulonephritis, serum sickness. Can be associated with vasculitis and systemic manifestations.

146
Q

Examples of type IV hypersensitivity disorders

A

Contact dermatitis (eg poison ivy, nickel allergy), graft vs host disease, multiple sclerosis, PPD test. Response is delayed and does not involve antibodies (vs types I, II, III).

147
Q

Allergic reaction to blood transfusion

A

It is a type I hypersensitivity reaction against plasma proteins in transfused blood. Causes urticaria, pruritus, wheezing, fever. Treat with antihistamines.

148
Q

Anaphylactic reaction to blood transfusion

A

It is a severe allergic reaction. IgA deficient individuals must receive blood products without IgA. Causes dyspnea, bronchospasm, hypotension, respiratory arrest, shock. Treat with epinephrine.

149
Q

Febrile nonhemolytic transfusion reaction

A

It is a type II hypersensitivity reaction. Host antibodies against donor HLA antigens and WBCs. Symptoms include fever, headaches, chills, and flushing.

150
Q

Acute hemolytic transfusion rection

A

Type II hypersensitivity reaction. Intravesicular hemolysis (ABO blood group incompatibility) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs). Causes fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria (intravascular hemolysis), jaundice (extravascular).

151
Q

Anti-ACh receptor

A

Myasthenia gravis

152
Q

Anti-basement membrane

A

Goodpasture syndrome

153
Q

Anticardiolipin

A

SLE, antiphospholipid syndrome

154
Q

Lupus anticoagulant

A

SLE, antiphospholipid syndrome

155
Q

anticentromere

A

Limited scleroderma (CREST syndrome-calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia)

156
Q

Anti-desmosome (anti-desmoglein)

A

Pemphigus vulgaris

157
Q

Anti-dsDNA

A

SLE

158
Q

Anti-Smith

A

SLE

159
Q

Anti-glutamic acid decarboxylase (GAD-65)

A

Type 1 diabetes mellitus

160
Q

Antihemidesmosome

A

Bullous pemphigoid

161
Q

Anti-histone

A

Drug-induced lupus

162
Q

Anti-Jo-1

A

Polymyositis, dermatomyositis

163
Q

Anti-SRP

A

Polymyositis, dermatomyositis

164
Q

Anti-Mi-2

A

Polymyositis, dermatomyositis

165
Q

Antimicrosomal

A

Hashimoto thyroiditis

166
Q

Antithyroglobulin

A

Hashimoto thyroiditis

167
Q

Antimitochondrial

A

primary biliary cirrhosis

168
Q

Antinuclear antibodies

A

SLE, nonspecific

169
Q

Antiparietal cell

A

pernicious anemia

170
Q

Ant-Scl-70 (anti-DNA topoisomerase I)

A

Scleroderma (diffuse)

171
Q

Anti-smooth muscle

A

Autoimmune hepatitis

172
Q

Anti-SSA (Anti-Ro)

A

Sjogren syndrome

173
Q

Anti-SSB (Anti-La)

A

Sjogren syndrome

174
Q

Anti-TSH receptor

A

Graves disease

175
Q

Anti-UI RNP (ribonucleoprotein)

A

Mixed connective tissue disease

176
Q

IgA anti-edomysial

A

Celiac disease

177
Q

IgA anti-tissue transglutaminase

A

Celiac disease

178
Q

MPO-ANCA

A

Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (Churg- Strauss syndrome)

179
Q

p-ANCA

A

Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (Churg- Strauss syndrome)

180
Q

PR3-ANCA

A

Granulomatosis with polyangiitis (Wegner)

181
Q

c-ANCA

A

Granulomatosis with polyangiitis (Wegner)

182
Q

Rheumatoid factor (IgM antibody that targets IgG Fc region)

A

Rheumatoid arthritis

183
Q

anti-CCP

A

Rheumatoid arthritis (more specific than rheumatoid factor)

184
Q

X-linked (Burton) agammaglobulinemia

A

Due to a result in BTK, a tyrosine kinase gene, which causes there to be no B-cell maturation. (in Boys). Leading to recurrent bacterial and enteroviral infections after 6 months of age (due to a decrease in maternal IgG). There are absent B cells in peripheral blood, causing a decrease in Ig of all classes. There are also absent/scanty lymph nodes and tonsils.

185
Q

Selective IgA deficiency

A

The cause is unknown. It is the most common immunodeficiency. In majority of people it is asymptomatic. It can lead to Airway and GI infections, Atopy (hyper-allergic), Anaphylaxis to IgA-containing products. There is a decrease in IgA with normal IgG, IgM levels.

186
Q

Common variable immunodeficiency

A

Due to a defect in B-cell differentiation. There are many causes. It can be acquired in the 20’s-30’s; there is an increase risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infections. There are a decrease in plasma cells and Ig.

187
Q

Thymic aplasia (DiGeorge syndrome)

A

22q11 deletion; leads to a failure to develop 3rd and 4th pharyngeal pouches, causing an absence in thymic and parthyroid glands. Patients present with tetany (hypocalcemia), recurrent viral/fungal infections (T-cell deficiency), conotruncal abnormalities (eg tetralogy of fallot, truncus arteriosus). Findings include a decrease in T cells, PTH, and Ca. There is an absent thymic shadow on CXR. 22q11 deletion detected by FISH.

188
Q

IL-12 receptor deficiency

A

Causes a decrease Th1 response. It is autosomal recessive. It presents as disseminated mycobacterial and fungal infections; may present after administration of BCG vaccine. There will be a decrease in IFN-gamma.

189
Q

Autosomal dominant hyper IgE syndrome (Job syndrome)

A

It is due to a deficiency of Th17 cells due to a STAT3 mutation, leading to impaired recruitment of neutrophils to sites of infection. Presentation is FATED: coarse Facies, cold (noninflamed) staphylococcal Abscesses, retained primary Teeth, increase in IgE, Dermatologic problems (eczema). Serum shows an increase in IgE and a decrease in IFN-gamma.

190
Q

Chronic mucocutaneous candidiasis

A

Causes T-cell dysfunction. There are many causes. Presents as noninvasive Candida albicans infections of skin and mucous membranes. There are absent in vitro T-cell proliferation in response to Candida antigens. There is also an absent cutaneous reaction to Candida antigens.

191
Q

Severe combined immunodeficiency

A

There are several types including a defect in IL-2R gamma chain (most common, X-linked) and adenosine deaminase deficiency (autosomal recessive, which leads to the accumulation of ATP and dATP. Excess dATP inhibits ribonucleotide reductase and DNA synthesis, resulting in decreased lymphocyte counts. It presents as failure to thrive, chronic diarrhea, and thrush. There are also recurrent viral, bacterial, fungal, and protozoal infections. Treatment includes bone marrow transplant (no adaptive mediated immune rejection). Lab findings will show a decrease in T-cell receptor excision circles (TRECs). There will also be an absence of a thymic shadow on CXR, germinal centers on lymph node biopsy, and T cells on flow cytometry.

192
Q

Ataxia-talengiectasia

A

Due to a defect in ATM gene, which leads to a failure to repair double strand DNA breaks causing cell cycle arrest. It causes a triad of cerebellar defects (Ataxia), spider Angiomas (telangiectasia, and IgA deficiency. Lab findings will show an increase in alpha fetoprotein, a decrease in IgA, IgG, and IgE, lymphopenia, and cerebellar atrophy.

193
Q

Hyper IgM syndrome

A

It is most commonly due to a defective CD40L on Th cells, which leads to defective class switching. It is x linked recessive. It presents with severe pyogenic infections early in life and opportunistic infections such as Pneumocystis, Cryptosporidium, and CMV. Lab findings will show an increase of IgM and a large decrease in IgG, IgA, and IgE.

194
Q

Wiskott-Aldrich syndrome

A

Due to a mutation in WAS gene (x-linked recessive), which makes T cells unable to reorganize actin cytoskeleton. Presents as WATER: Wiskott-Aldrich: Thrombocytopenia, Eczema, Recurrent infections. There is also an increase risk of autoimmune disease and malignancy. Lab findings will show decrease to normal levels of IgG and IgM, an increase in IgE and IgA, and fewer and smaller platelets.

195
Q

Leukocyte adhesion deficiency (type 1)

A

Due to a defect in LFA-1 integrin (CD18) protein on phagocytes; impaired migration and chemotaxis. It is autosomal recessive. It presents as recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, and delayed separation of umbilical cord (over 30 days). Lab findings will show an increase in neutrophils in serum but an absence of neutrophils at the infection sites.

196
Q

Chediak-Higashi syndrome

A

It is due to a defect in lysosomal trafficking regulator gene (LYST), which leads to microtubule dysfunction in phagosome-lysosome fusion. It is autosomal recessive. Histology findings will show giant granules in granulocytes and platelets. There will also be pancytopenia and mild coagulation defect.

197
Q

Chronic granulomatous disease

A

Due to a defect of NADPH oxidase, which leads to a decrease in reactive oxygen species (eg superoxide) and a decrease of respiratory burst in neutrophils. X-linked recessive is most common. It presents as an increase susceptibility to catalase positive organisms (Need PLACESS): Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E coli, S aureus, Serratia. Lab findings will show an abnormal dihydrohodamine on flow cytometry and a negative nitroblue tetrazolium dye reduction test.

198
Q

Common bacterial infections in a immunodeficiencies with decrease T cells

A

Sepsis

199
Q

Common viral infections in a immunodeficiencies with decrease T cells

A

CMV, EBV, JCV, VZV, chronic infection with respiratory/ GI viruses. B-cell deficiencies tend to produce recurrent bacterial infections, whereas T-cell deficiencies produce more fungal and viral infections.

200
Q

Common fungal/parasites infections in a immunodeficiencies with decrease T cells

A

Candida (local) and Pneumcystitis pneumonia

201
Q

Common bacterial infections in a immunodeficiencies with decrease B cells

A

Encapsulated; SHiNE SKiS: Streptococcus pneumoniae, Haemophilus influenzae type B, Neisseria emingitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, group B Strep. B-cell deficiencies tend to produce recurrent bacterial infections, whereas T-cell deficiencies produce more fungal and viral infections.

202
Q

Common viral infections in a immunodeficiencies with decrease B cells

A

Enteroviral encephalitis, poliovirus (live vaccine contraindicated)

203
Q

Common fungi/parasites infections in a immunodeficiencies with decrease B cells

A

GI giardiasis (no IgA)

204
Q

Common bacterial infections in a immunodeficiencies with decrease granulocytes

A

Staphylococcus, Burkholderia cepacia, Pseudomonas aeruginosa, Serratia, Nocardia.

205
Q

Common viral infections in a immunodeficiencies with decrease granulocytes

A

Granulocyte deficiency does not predispose patients to viral infections.

206
Q

Common fungi/parasites infections in a immunodeficiencies with decrease granulocytes

A

Candida (systemic), Aspergillus

207
Q

Common bacterial infections in a immunodeficiencies with decrease complement

A

Encapsulated species with early component deficiencies. Encapsulated; SHiNE SKiS: Streptococcus pneumoniae, Haemophilus influenzae type B, Neisseria emingitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, group B Strep. Neisseria with late component (MAC) deficiencies.

208
Q

Common viral infections in a immunodeficiencies with decrease complement

A

Complement deficiency does not predispose patients to viral infections.

209
Q

Common fungi/parasites infections in a immunodeficiencies with decrease complement

A

Complement deficiency does not predispose patients to fungi/parasites infections.

210
Q

Autograft

A

Graft from self

211
Q

Syngeneic graft (isograft)

A

Graft from identical twin or clone

212
Q

Allograft

A

Graft from nonidentical individual of same species.

213
Q

Xenograft

A

Graft from different species

214
Q

Hyperacute transplant rejection

A

Onset is within minutes. It is due to pre-existing recipient antibodies react to donor antigen (type II hypersensitivity reaction), which activates complement. It causes widespread thrombosis of graft vessels, which causes ischemia and necrosis. The graft must be removed.

215
Q

Acute transplant rejection

A

Onset is weeks to months. It occurs due to CD8+ T cells activated against donor MHCs and development of antibodies after the transplant (as opposed to preformed antibodies in a hyperacute rejection). It causes vasculitis of graft vessels with dense interstitial lymphocytic infiltrate. It can be prevented or reversed with immunosuppressants.

216
Q

Chronic transplant rejection

A

Onset is months to years. It occurs due to CD4+ T cells responding to recipient APCs presenting donor peptides, including allogenic MHC. There are both cellular and humoral components. Recipient T cells react and secrete cytokines leads to proliferation of vascular smooth muscle and parenchymal fibrosis. It is dominated by arteriosclerosis.

217
Q

Graft versus host disease transplant rejection

A

Onset varies. It occurs due to grafted immunocompetent T cells proliferating in the immunocompromised host, which reject host cells with “foreign” proteins leading to severe organ dysfunction. It causes maculopapular rash, jaundice, diarrhea, hepatosplenomegaly. It is usually due to bone marrow or liver transplants, which are rich in lymphocytes. It can potentially be beneficial in bone marrow transplant for leukemia because it can lead to a graft versus tumor effect.

218
Q

Immunosuppressants

A

Agents that block lymphocyte activation and proliferation. They can reduce acute transplant rejection by suppressing cellular immunity. They are frequently combined to achieve efficacy with a decrease in toxicity. Chronic suppression increases the risk of infection and malignancy.

219
Q

Mechanism of cyclosporine

A

Calcineurin inhibitor; binds cyclophilin. Blocks T-cell activation by preventing IL-2 transcription.

220
Q

Use of cyclosporine

A

Prophylactic transplant rejection, psoriasis, and rheumatoid arthritis.

221
Q

Toxicity of cyclosporin

A

Nephrotoxicity is the most important toxicity. Hypertension, hyperlipidemia, neurotoxicity, gingival hyperplasia, and hirsutism. Both calcineurin inhibitors are highly nephrotoxic.

222
Q

Mechanism of tacrolimus (FK506)

A

Calcineurin inhibitor; binds FK506 binding protein (FKBP). It blocks T-cell activation by preventing IL-2 transcription.

223
Q

Use of tacrolimus (FK506)

A

Transplant rejection prophylaxis

224
Q

Toxicity of tacrolimus (FK506)

A

Similar to cyclosporine, there is an increase risk of diabetes and neurotoxicity; no gingival hyperplasia or hirsutism. Both calcineurin inhibitors are highly nephrotoxic.

225
Q

Mechanism of sirolimus (rapamycin)

A

mTOR inhibitor; bindsFKBP. Blocks T-cell activation and B-cell differentiation by preventing response to IL-2.

226
Q

Use of sirolimus (rapamycin)

A

Kidney transplant rejection prophylaxis

227
Q

Toxicity of sirolimus (rapamycin)

A

Anemia, thrombocytopenia, leikopenia, insulin resistance, hyperlipidemia; not nephrotoxic. Kidney “sir-vives.” Synergistic with cyclosporin. Also used in drug eluting stents.

228
Q

Mechanism of daclizumab

A

Monoclonal antibodies; block IL-2R

229
Q

Use of daclizumab

A

Kidney transplant rejection prophylaxis

230
Q

Toxicity of daclizumab

A

Edema, hypertension, and tremor

231
Q

Mechanism of basiliximab

A

Monoclonal antibodies; block IL-2R

232
Q

Use of basiliximab

A

Kidney transplant rejection prophylaxis

233
Q

Toxicity of basiliximab

A

Edema, hypertension, and tremor

234
Q

Mechanism of azathioprine

A

Antimetabolite precursor of 6-mercaptopurin. Inhibits lymphocyte proliferation by blocking nucleotide synthesis. Azathio-purine.

235
Q

Use of azathioprine

A

Transplant rejection prophylaxis, rheumatoid arthritis, Crohn disease, glomerulonephritis, and other autoimmune conditions.

236
Q

Toxicity of azathioprine

A

Leukopenia, anemia, thrombocytopenia. 6-MP degraded by xanthine oxidase; toxicity increases by allopurinol.

237
Q

Mechanism of glucocorticoids

A

Inhibit NF-kB. Suppresses both B- and T-cell function by decreasing transcription of many cytokines.

238
Q

Use of glucocorticoids

A

Transplant rejection prophylaxis (immunosuppression), many autoimmune disorders, inflammation.

239
Q

Toxicity of glucocorticoids

A

Hyperglycemia, osteoporosis, central obesity, muscle breakdown, psychosis, acne, hypertension, cataracts, avascular necrosis. Can cause iatrogenic Cushing syndrome.

240
Q

Aldesleukin

A

IL-2, used to treat renal cell carcinoma and metastatic melanoma.

241
Q

Epoetin alfa

A

Erythropoietin, used to treat anemias (especially in renal failure).

242
Q

Filgrastim

A

G-CSF, used for recovery of bone marrow

243
Q

Sargramostim

A

GM-CSF, used for recovery of bone marrow

244
Q

IFN-alpha

A

used to treat chronic hepatitis B and C, Kaposi sarcoma, and malignant melanoma.

245
Q

IFN-beta

A

Used to treat multiple sclerosis

246
Q

IFN-gamma

A

Used to treat chronic granulomatous disease

247
Q

Romiplostim

A

Thrombopoietin, used to treat thrombocytopenia

248
Q

Eltrombopag

A

Thrombopoietin, used to treat thrombocytopenia

249
Q

Oprelvekin

A

IL-11, used to treat thrombocytopenia

250
Q

Alemtuzumab

A

Antibody that targets CD52. Used to treat chronic lymphocytic leukemia (CLL). “Alymtuzumab”- chronic lymphocytic leukemia.

251
Q

Bevacizumab

A

Antibody that targets VEGF. Used to treat colorectal cancer and renal cell carcinoma.

252
Q

Cetuximab

A

Antibody that targets EGFR. Used to treat stage IV colorectal cancer and head and neck cancer.

253
Q

Rituximab

A

Antibody that targets CD20. Used to treat B-cell non-Hodgkin lymphoma, CLL, rheumatoid arthritis, and idiopathic thrombocytopenic purpura (ITP)

254
Q

Trastuzumab

A

Antibody that targets HER2/neu. Used to treat breast cancer. HER2- tras2zumab.

255
Q

Adalimumab

A

Antibody that targets soluble TNF-alpha. Used to treat IBD, rheumatoid arthritis, ankylosing spondylitis, and psoriasis.

256
Q

Etanercept

A

It is decoy TNF-alpha receptor and not monoclonal antibody.

257
Q

Infliximab

A

Antibody that targets soluble TNF-alpha. Used to treat IBD, rheumatoid arthritis, ankylosing spondylitis, and psoriasis.

258
Q

Eculizumab

A

Antibody that targets complement protein C5. Used to treat paroxysmal nocturnal hemoglobinuria.

259
Q

Natalizumab

A

Antibody that targets alpha4-integrin. Used to treat multiple sclerosis and Crohn disease. α4-integrin is required for white blood cells adhesion in order to move into organs. There is a risk for progressive multifocal leukoencephalopathy (PML) in patients with JC virus.

260
Q

Abciximab

A

Antibody that targets platelet glycoproteins IIb/IIIa. Used to treat antiplatelet agent for prevention of ischemic complications in patients undergoing percutaneous coronary intervention. IIb x IIIa equals “ab-six-imab”

261
Q

Denosumab

A

Antibody that targets receptor activator of nuclear factor kappa-B ligand (RANKL). Used to treat osteoporosis; inhibits osteoclast maturation (mimics osteoprotegerin). DenOSumab affects OSteoclasts.

262
Q

Dioxin immune Fab

A

Antibody that targets digoxin. Used as an antidote for digoxin toxicity.

263
Q

Omalizumab

A

Antibody that targets IgE. Used to treat allergic asthma; prevents IgE binding to FcERI (high-affinity receptor for the Fc region of immunoglobulin E).

264
Q

Palivizumab

A

Antibody that targets RSV F protein. Used as a RSV prophylaxis for high-risk infants. PaliVIzumab- VIrus.

265
Q

Ranibizumab

A

Antibody that targets VEGF. Used to treat neovascular age-related macular degeneration.

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