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ACVIM Reading List > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the 2 main components of the immune system?

A
  1. Innate Immunity

2. Adaptive Immunity

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2
Q

What is the innate immune system and name several effector cells?

A

Available for immediate defense with no prior exposure required!
Components: Physical and chemical barriers, Circulating cells, complement, cytokines, interferons, defensins
Cells: Neutrophils, eosinophils, mast cells, macrophages, dendritic cells

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3
Q

What components of complement lead to more inflammation?

A

Anaphylatoxins = C3a and C5a

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4
Q

What is the final outcome of complement activation?

A

Stimulates activation of terminal complement components (C5b-C9-membrane attack complex)

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5
Q

What is a TLR?

A

Toll-like receptor - recognizes intracellular and extraceullar bacteria/virus
On neutrophils - Result in cytokine production = Inflammatory response
TLR2 - Bacterial lipopeptide
TLR4 - LPS

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6
Q

What is a NLR?

A

NOD-like receptor - recognizes intracellular bacteria/virus
On neutrophils - Result in cytokine production = Inflammatory response
NLRs = Bacterial lipopeptides

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7
Q

What are cytokines and chemokines?

A

Cytokine: Proteins that are made by affector cells to affect behavior of other cells
Chemokines: Cytokines that are important for chemotaxis

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8
Q

Name the 3 cytokines important for inflammation/fever.

A

IL-1
IL-6
TNFa

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9
Q

What are 2 major chemokines?

A

IL-8

CXCL1

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10
Q

What are the 3 major cell types of adaptive immunity?

A

Lymphocytes (B and T cell)

Antigen presenting cells

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11
Q

What is humoral immunity?

A

B cells recognize antigen through surface bound Ig> Once activated to become a plasma cell or long-lived memory cell = Secrete Ig, which bind pathgens in extracellular space - leading to their destruction through phagocytosis and complement binding

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12
Q

What is cell mediated immunity?

A

T cells (via T cell receptors) recognize INTRACELLULAR antignes on cell surface of antigen presenting cells (DO NOT bind free antigen, unlikely B cells)! Based on specialized cellular gylocproteins (gene cluster) = Major Histocompatibility Complex (MHC). Once activated, T cell differentiate into cytotoxic cells (CD8+) or helper cells (CD4+)

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13
Q

Cytotoxic T cells are CD___+.

A

CD8+

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14
Q

Helper T cells are CD___+.

A

CD4+

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15
Q

Name 3 antigen presenting cells.

A

Macrophages, dendritic cells, B cells

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16
Q

What is the role of an antigen presenting cell?

A

Along with MHC internalize, process, and present antigen+MHC on their cell surface to be recognized by T cells

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17
Q

Where do B cells and T cells “live” in the body?

A

B cells = BM

T cells = Thymus

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18
Q

What is colonal selection?

A

Single lymphocyte progenitor produces millions of cells with DIFFERENT and SPECIFIC antigen receptor on each cells - occurs through rearrangement of gene segments in variable region of antigen receptors EACH LYMPHOCTE EXPRESSES ONLY 1 SPECIFIC RECEPTOR

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19
Q

What happens once a lymphocyte is activated?

A

Interaction of the receptor with a foreign antigen with sufficient binding = activates lymphocyte → Produces CLONES with the SAME SPECIFIC receptor. Clones are known as effector cells, capable of eliminating antigens

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20
Q

How do T cells differ from B cells in term of differentiation?

A

T cells are MHC restricted!! T cells can recognize foreign antigen only in form of peptide bound to a self MHC molecule on APC.

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21
Q

What is positive selection?

A

T cells must be able to recognize the body’s own MHC molecules (since they are MHC restricted and can only recognize a foreign antigen when it is bound to a self MHC molecule on an APC)

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22
Q

What is negative selection?

A

T cells must be able to recognize self peptides bound to self MHC molecules and become self tolerant. Cells binding with high affinity are deleted = negative selection

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23
Q

What happens when a T cell fails positive and negative selection?

A

It undergoes apoptosis

Estimated that 98% of immature T cells die this way

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24
Q

Which lymphocyte is produced throughout life?

A

B cells

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25
Q

What are the major steps in lymphocyte migration to sites of inflammation?

A
  1. Teter and rolling: Based on P and E selectins on endothelial cells or L-selectin (LN). Rolling mediated by binding of integrins (WBCs) to VCAMS or ICAMS (on endothelial cells)
  2. Activation: Baed on chemokines (IL-8)
  3. Arrest: Based on b integrins to ICAMs asn MadCAMs
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26
Q

What portion of an antibody binds to the antigen?

A

Variable region (Fab) - varies extensively to match antigen variety

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27
Q

What portion of an antibody binds to the APC?

A

Constant region (Fc) - leads to recruitment of additional immune cells and destruction of pathogen

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28
Q

What determines the antibody isotype and name the 5 types of antibodies?

A

Constant (Fc) region determines the isotype

IgM (pentamer), IgG, IgD, IgE, IgA (Dimer)

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29
Q

How is a B cell activated?

A

Antigen binding to transmembrane B Cell antigen receptor stimulates clonal expansion (lots of phosphorylations) and differentiation to an antibody secreting plasma cell (short lived) or memory cells (long-lived) occurs

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30
Q

What is a common leukocyte antigen?

A

CD45 (present on all WBCs) - Transmembrane surface glycoprotein

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31
Q

What is the main function of the MHC?

A

To process and present pathogenic peptides to 2 distinct classes of T cells

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32
Q

What is the difference btwn MCH I and MCH II molecules?

A

MHC I: a chain and b2 microglobulin - Does NOT cross the membrane = Expressed on majority of nucleated cells
MCH II: a and b chains - crosses the membrane = Mainly expressed in APCs and in thymus (self recognition)

Great polymorphorism is present in MCH molecules

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33
Q

What is DLA?

A

Dog Leukocyte Antigen

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34
Q

What is the role of MCH Class I in antigen processing and presentation?

A

Presents peptides to CD8+ (cytotoxic, killer cells)
Pathogens that are found in cytosol (viruses, tumor antigen, some bacteria) = Cell death
Cytosolic pathgenic proteins are degraded by proteosomes and delivered to ER where MHC I molecule is ready , peptide binding occurs = MHC I: Peptide complex transported to surface where it is exposed to CD8+ T cells

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35
Q

What is the role of MCH Class II in antigen processing and presentation?

A

Present peptides to CD4+ (T helper 1 or 2). Th1 - Acitvate inflammatory cells to kill intravesicular pathogens, Th2 - activate B cells to secrete Ig to eliminate extracellular bacteria/toxin
Antigen exists or is transported to intracellular vesicle and degraded into peptides, which fuse with MCH II and move to cell surface and exposed to CD4+ cells

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36
Q

What is the difference btwn Th1 and Th2?

A 
Th1 = Activate inflammatory cells to kill pathogen (intravesicular)
Th2 = Activate B cells to produce Ig (extracellular)
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37
Q

What are the components of the T cell receptor complex?

A

Resembles the Fab portion of Ig (contains constant and variable region in a and b chains
Assoicated with CD3 complex (intracellular signaling) and CD45 (on all WBCs)
Co-receptor: CD4 or CD8 (some carry both)

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38
Q

What is the superantigen?

A

Binds ACROSS the MCH:T cell receptor (without processing) = Activation leads to massive production of cytokines by CD4 cells that leads to SIRS!!!
Bacteria (Stap enterotoxins, and some viral proteins)

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39
Q

Discuss the activation of naïve T Cells to effector T cells.

A
  1. Naïve T cells migrate to peripheral lymph organs were they are exposed to APCs (MP, dendritic cells, B cells) - Encounter of T cells with an antigen (on APC surface) = Primary immune response
  2. Recognition of MCH: Antigen complex
  3. CO-STIMULATORY SIGNAL delivered by same APC - binding of cell surface molecule B7 found on APC to CD 28 on T cell
  4. Activated T cells makes IL-2 = Drives T cell growth and clonal proliferation = Armed effector cell that is capable of carrying out cytotoxic or helper functions WITHOUT co-stimulation
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40
Q

What 2 steps are required for T cell activation?

A
  1. Recognition of MCH: Antigen complex
  2. CO-STIMULATORY signal delivered by SAME APC (Binding of cell surface molecule B7 found on APC to CD 28 found on T cell)
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41
Q

Which cytokines result in Th1 vs Th2 T cell development?

A

IL-12 drives inflammatory or Th1 response (Cell mediated immunity)

IL-4 drives a helper or Th2 response (humoral immunity)

42
Q

What cytokines are seen with Th1 cells?

A

IFN gamma, TNF alpha and beta, IL-2

43
Q

What is IFN gamma and TNF alpha?

A

Cytokines that are macrophage activators

44
Q

What is IFN gamma?

A

Cytokine that blocks viral replication

45
Q

What is TNF beta?

A

Cytokine that is cytotoxic

46
Q

What is IL-2?

A

Cytokine that is needed for growth of Th1 cells

47
Q

What are Th2 cytokines?

A

IL-4, 5, 6, 10, TGF beta

48
Q

What is IL-4?

A 
Cytokine that is a growth factor for Th2 cells and B cells
Induced class switch from IgG to IgE
49
Q

What is IL-5?

A

Cytokines that induced IgA switch and activates eosinophils

50
Q

What is IL-6?

A

Proinflammatory cytokine - induced acute phase response

51
Q

What is IL-3?

A

Cytokine that is hematopoetic growth factor that activates mast cells

52
Q

Name 4 primary mechanisms of the humoral immune response.

A
  1. Neutralization: Binding to extracellular pathogens to inhibits toxic effects
  2. Opsonization - facilitation of uptake and destruction of pathogens by Ig binding to pathogen at Fab region and binding to the Fc receptor of phagocytic cell
  3. Complement Activation - Leads to enhanced opsonization and cell lysis
  4. Functions as APC with MCH II
53
Q

Which cell type plays a role in isotype switching of B cells?

A

Th2 cells

54
Q

What is a plasma cell?

A

A B cells that has differentiated. Lacks surface Ig for bindings and contains low to zero MHC II = Plasma cells are no longer able to interact with antigen OR T cells
Ig secretion INDEPENDENT of these factors
Life span = 4 wks

55
Q

What is immunologic memory?

A

Ability of immune system to respond more rapidly and effectively to a pathogen that is has encountered before. Due to pre-existence of clonally expanded population of antigen specific lymphocytes (controversial how memory is maintained)
Gives ability to vaccinate or immunize

56
Q

What is the primary antibody response?

A

IgM and then it changes to IgG +/- other subtypes

57
Q

Name 5 Fc receptor bearing cells.

A

Macrophages, PMN, nautral killer cells, eosinophils, mast cells = All secrete toxic mediators when Fc receptor engaged

58
Q

What are the most effective opsonins?

A

Antibodies and complement

59
Q

How do dogs and cats differ in clearing bacteria from bloodstream?

A

Dog - Use Kupfer cells (macrophages) in the liver

Cat - Use pulmonary intravascular macrophages

60
Q

What are the 3 pathways of complement?

A
  1. Alternative Pathway (innate)
  2. Lectin Pathway (innate)
  3. Classical Pathway (adaptive)
61
Q

How are the innate complement pathways activated?

A

Recognizing PAMPs

62
Q

How is the adaptive/classical pathway of complement activated?

A

Antibodies that are bound to foreign antigen

63
Q

Which part of complement results in opsonization of microbes?

A

C3b

64
Q

Which part of complement results in inflammation?

A

C5a (chemoattractant)

65
Q

What are the 3 main steps of complement activation?

A
  1. Complement must be activated (PAMP or antibody:antigen)
  2. C3b must be generated
  3. Terminal complement complex assembled through amplification pathway
66
Q

What is an example of a complement deficiency that is seen in dogs?

A

Canine C3 deficiency = Increased susceptibility to infections
Seen in colony of Brittany Spaniels (autosomal recessive)

67
Q

What is the shock organ of the dog? Symptoms? And Major mediators?

A

Hepatic veins
Collapse, Dyspena, Diarrhea, Vomiting
Histamine, Leukotrienes, Prostaglandins

68
Q

What is the shock organ of the cat? Symptoms? And Major mediators?

A

Respiratory Tract (intestines)
Dyspnea, Vomiting, Diarrhea, Pruitus (head/neck)
Histamine, Leukotrienes

69
Q

What is a type I hypersensitivity?

A

Immediate Hypersensitivity
Results from IgE attached to mast cell (proclud earlier from Th2 response) is cross-linked by antigen = = Degranulation of mast cell = Acute inflammation (anaphylaxis)

70
Q

Which of the DEA are clinically significant?

A

DEA 1 antigen (expressed by 60% of dogs, no naturally occurring antibodies)
DEA 1.1 (33-45% of dogs, universal recipients; if negative for DEA 1.1 = universal donor
DEA 1.2

71
Q

What is the major blood group system in cats?

A 
AB system (glycolipids) 
A = 75-95% of cats (only 35% have anti-B  IgM or IgG)
B = 5-25% of cats (of these cats 95% have anti-A IgM
AB = < 1% of cats
72
Q

Why is cross-matching essential in cats?

A

If a B cat gets A blood they will go into shock and likely will die!

73
Q

Name another blood types in cats, besides AB system?

A

Mik blood antigen

74
Q

What is Type II hypersensitvity?

A

Cytotoxic Hypersensitivity
Antibody mediated = Antibodies and complement destroy normal cells
IMHA, incompatible blood transfusion

75
Q

What is Type III hypersensitivity?

A

Immune Complex Formation
Soluble antigens and antibodies combine to form immune complexes that can bind with complement and get stuck in ““filter”” areas (capillaries, joints, kidneys) = Activates neurophils = Inflammation/tissue destruction
Glomerulonephritis and Polyarthritis

76
Q

What us Type IV hypersensitivity?

A

Delayed hypersenstivity
3 types: Th1 cells (activated MPs), Th2 cells (activated eosinophils, IgE), Cytotoxic T cells activation
Tubuculin Rxn, allergic contact dermatitis (Stevens-Johnson syndrome)

77
Q

What is the purpose of the Coomb’s test?

A

To detect antibody and complement on RBCs

78
Q

What does the regent for the Coomb’s contain?

A

Anti-IgG, anti-IgM, and anti-C3 (species specific)

79
Q

What is the prozone effect?

A

Relative excess of antiglobulin in relation to antigen (Ig or C3 on RBCs) at lower antisera dilutions resulting in decreased cross-linking of RBCs causing failure to agglutinate at low antisera dilutions

80
Q

What helps to increase the sensitivity of the Coomb’s test?

A

Use of monovalent reagents, increased dilutions of antiglobulin to avoid a prozone effect, and testing at 4C

81
Q

What is the MOA of glucocorticoids?

A
  • Bind to cytosolic glucocorticoid receptor (GR), translocate to nucleus and binds to specific DNA sequence (glucocorticoid responsive elements) - enhance and inhibit transcription of genes
  • Anti-inflammatory: Stabilization of cell membranes of granulocytes, mast cells, and monocytes-MP, inhibition of phospholipase A2 (prevent release of arachidonic acid metabolites - COX and LOX pathways)
  • Prevent release of cytokines IL-1 and IL-6 = proinflammatory
  • Effects on complement and RAPID downregulation of Fc receptor expression on MP (reducing phagcytosis of opsonized RBCs and plts), esp with IM dz
82
Q

What is the MOA of azathioprine?

A
  • Cytotoxic synthetic imidzaole derivative of 6-mercaptopurine (6MP) - thiopurines that interfere with purine synthesis = BAD nucleotides = NO DNA or RNA made, mitosis and cell metabolism is disrupted
  • "”Lead - in”” time of 11 days prior to clinical effects, can have lag period for up to 3-5 weeks
  • Cell Mediated Immunity - Reduction in lymphocytes and T cell dependent antibody production
  • Synergistic effects with steroids, allows for rapid taper of steroids (““steroid sparing effect””)
83
Q

What are the 4 major side effects of azathioprine?

A
  • Myelosupression
  • Acute pancreatitis
  • Hepatopathy
  • Gastrointestinal Distress
84
Q

What immunosupressant is there a documented breed variation?

A

Azathioprine: • Converted in liver (and other tissues) to 6MP
• Thiopurine methyltansferase (TPMT) - enzyme in metabolism of 6MP
• Measure it in RBCs
• Variable in TPMT levels correlated with clinical outcomes in humans (high level = reduced efficacy; low level = risk of bone marrow toxicity
• Document breed variations (Low levels in Giant Schnauzers, thus watch for toxicity, and high levels in Alaskan malamutes)

85
Q

What occurs when giant schnauzers are given azathioprine?

A

Low levels of thiopurine methyltransferase (TPMT) = Watch for toxicity!!

86
Q

What occurs when Alaskan malamutes are given azathioprine?

A

High levels of thiopurine methyltransferase (TPMT) = Watch for reduced efficacy!!

87
Q

What is the MOA of cyclophosphamide?

A
  • Cytotoxic alkylating agent, cross-links DNA, thus preventing separation
  • Suppresses CMI and humoral immunity
88
Q

Name 2 side effects of cyclophosphamide?

A

Hemorrhagic cystitis

Myelosupression

89
Q

What is the MOA of cyclopsorine?

A
  • VERY POTENT T CELL INHIBITOR
  • ***Blocks transcription of genes required for T cell activation - IL-2 production is blocked
  • Binds to cyclophilin (high concentration in cytoplasma of T cells) to form complex that prevents activation of calcineurin (that normally occurs when T cell receptor engages an antigen and triggers influx of Ca into cell)
  • Normally calcineurin acts as nuclear factor to induce cytokine gene transcription
  • Reduced IL-2 production = reduced clonal proliferation of T cells, and thus B cells
90
Q

Name possible side effects of cyclosporine?

A

• Gastrointestinal signs (transient)
• SERIOUS opportunistic infections
• Emergence of neoplasia
Gingival hyperplasia

91
Q

What is the MOA of human IV Ig?

A
  • Competitively inhibits the binding of K9 IgG to monocytes by saturation of Fc receptors = prevents phagocytosis of antibody coated RBCs and platelets
  • Use in IMHA and IMTP
92
Q

What is the MOA of danazol?

A
  • Synthetic Androgen
  • Downregulates MP Fc receptor expression
  • Reduced antibody binding to RBCs
  • Stabilizes RBCs membranes
93
Q

What is the MOA of vincristine for IMTP?

A
  • Low doses to increase platelet counts by stimulating megakaryocytes and impairs phagocytosis of opsonized platelets by impairing microtubule assembly MP
  • Unknown effect on platelet function
94
Q

What is a side effect of danazol in dogs?

A

Hepatotoxic (dogs)

95
Q

What is the MOA of leflunomide?

A
  • Isoxazole immunomodulating drug
  • Primary metabolite - REVERSIBLY inhibits dihydro-orotate dehydrognease (RATE LIMITING ENZYME in de novo pyrimidine synthesis)
  • High concentrations = Inhibits cytokine and growth factor receptor associated tyrosine kinase activity
  • T and B cell proliferation inhibited
96
Q

What are potential side effects with leflunomide?

A
  • Hepatotoxicity

* Myelotoxicity

97
Q

What is the MOA of mycophenolate?

A
  • Metabolized in plasma and liver to MYCOPHENOLIC ACID (MPA)
  • Reversible inhibitor of inosine monophospahte dehydrogenase (IMPDH) - KEY ENZYME in purine biosynthesis
  • Essential for lymphocyte proliferation (T and B cells proliferation, differentiation of Tc Cells and antibody production)
98
Q

Which immunosuppressive drug interferes with pyrimidine synthesis?

A

Leflunomide

99
Q

Which immunosuppressive drug interferes with purine synthesis?

A

Azathioprine

Mycophenolate

100
Q

How quickly can mycophenolate work?

A

Parenteral form - RAPID inhibition of IMPDH and thus immunosupression - 2-4 hours after dosing (FAST!!)

101
Q

What is the MOA of lipsome-encapsulated clodronate?

A
  • Bisphosphate (management of hypercalcemia associated with Vit B intoxication)
  • Preferentially phagocytosed by MP and dendritic cells - APOPTOSIS
  • Induced killing in splenic MP and dendritic cells
  • Inhibits clearance of opsonized RBCs in normal dogs
  • ROLE: Treat antibody mediated cytopenias where MP are key
  • Stops RBC and platelet destruction while gaining time for slower acting agents

ACVIM Reading List (27 decks)

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