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Immunology > Exam 1 Material > Flashcards

Exam 1 Material Flashcards

1
Q

Why is the immune system so important?

A
  1. Protects animals against microbial invasion, essential for life
  2. Ensures freedom from invasion via innate and adaptive immunity
  3. Utilizes complex, interacting networks of defense mechanisms
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2
Q

What century was the smallpox variolation?

A

12th century

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3
Q

What year was Rinderpest inoculations?

A

1754

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4
Q

What year was Edward Jenner’s cowpox experiment; coined “vaccination”?

A

1798

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5
Q

What year was Pasteur’s fowl cholera experiment; anthrax and rabies vaccines?

A

1879

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6
Q

Who proved dead organisms can create effective vaccines? Hint: 2 names

A

Daniel Salmon and Theobald Smith

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7
Q

Who found bacterial products that also provided protection? Hint: 2 names

A

Von Behring and Kitasato

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8
Q

Define commensal

A

Colonize surfaces, non-invasive, and harmless

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9
Q

Define pathogens

A

Causes disease and there are primary and opportunistic pathogens

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10
Q

Define primary pathogens

A

Cause disease at any dose

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11
Q

What’s an example of a primary pathogen?

A

HIV

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12
Q

Define opportunistic pathogen

A

Cause disease in high doses

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13
Q

What is an example of opportunistic pathogen?

A

Mannheimia hemolytica

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14
Q

What is innate Immunity?

A
  • Rapid, non-specific, and immediate protection
  • Activated by PAMPs and DAMPs
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15
Q

What is adaptive Immunity?

A

Develops after exposure, specific, and has memory

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16
Q

What are the 5 components of Innate defense?

A
  1. Physical/Chemical Barriers
  2. Phagocytic and Sentinel Cells
  3. Complement System
  4. Cytokines
  5. Natural Killer (NK) Cells
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17
Q

What are physical/chemical barriers?

A

Skin, mucus membranes, microflora, stomach acid, antimicrobial peptides

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18
Q

What are phagocytic and sentinel cells?

A

Detect and eliminate pathogens

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19
Q

What are examples of phagocytic and sentinel cells?

A

Neutrophils, macrophages, dendritic cells

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20
Q

What is the complement system?

A

Enzyme cascade with antimicrobial activity

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21
Q

What are cytokines?

A

Protein messenger molecules that can act on other cells

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22
Q

What 3 components can cytokines act on or cell that produced it?

A
  • Proinflammatory cytokines
  • Chemokines
  • Interferons
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23
Q

Define chemokines

A
  • Cells migrate to sites of infection
  • Some produced by sentinel cells
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24
Q

Define proinflammatory cytokines

A
  • Secreted by sentinel cells (PAMPs & DAMPs)
  • Cause fever, lethargy, & loss of appetite
  • IL-1, IL-6, & TNF
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25
Q

Define interferons

A
  • Interferes with replication of viruses
  • Produced by virally infected cells
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26
Q

What are natural killer (NK) cells?

A

Kill infected/tumor cells lacking normal proteins

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27
Q

What is humoral immunity?

A
  • Mediated by antibodies (IgA, IgG, IgE, IgM) from B cells
  • Effective against bacterial invaders
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28
Q

What is Cell-Mediated Immunity (CMI)?

A

T cells (helper, cytotoxic) regulate responses and destroy infected cells

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29
Q

What are the two types of adaptive immunity?

A

Humoral immunity and cell-mediated immunity

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30
Q

What distinguishes innate from adaptive immunity?

A

Innate is rapid, non-specific, and lacks memory; adaptive is slower, specific, and has memory

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31
Q

Who coined the term “vaccination”?

A

Edward Jenner

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32
Q

What was the significance of Pasteur’s fowl cholera experiment?

A

It showed that aged cultures of Pasteurella multocida provided protection, launching immunology as a science

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33
Q

What do sentinel cells recognize to detect invasion?

A

Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs)

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34
Q

What are antibodies also known as?

A

Immunoglobulins (Ig)

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35
Q

Which type of adaptive immunity is directed primarily against bacterial invaders?

A

Humoral immunity

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36
Q

What distinguishes commensals from pathogens

A

Commensals colonize surfaces without causing disease, while pathogens cause disease

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37
Q

What is the role of proinflammatory cytokines?

A

They cause fever, lethargy, and loss of appetite

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38
Q

What type of cells do NK cells target?

A

Virus-infected cells and tumor cells

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39
Q

How does the adaptive immune system respond to a previously encountered pathogen?

A

It’s faster and has a more effective response

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40
Q

What’s a leukocyte?

A

Any white blood cell (WBC)

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41
Q

What’s a lymphocyte?

A

A type of WBC (T cell, B cell, NK cell)

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42
Q

What’s a granulocyte?

A

Polymorphonuclear cells (neutrophils, eosinophils, basophils)

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43
Q

What’s a mononuclear cells?

A

Lymphocytes or monocyte

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44
Q

What percentage of WBCs are neutrophils?

A

Neutrophils make up 55-90% of WBCs

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45
Q

What is the primary role of neutrophils?

A

They are the first responders to bacterial infections

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46
Q

What is the lifespan of a neutrophil?

A

Neutrophils live 8-10 hours in the blood and up to 2 days in total

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47
Q

What does “neutrophilia” indicate?

A

Elevated neutrophil levels, or neutrophilia, indicate a bacterial infection

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48
Q

What does “neutropenia” indicate?

A

Low neutrophil levels, or neutropenia, are often seen in viral infections

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49
Q

What is the role of basophils?

A

They are important in allergies and parasitic infections due to their inflammatory mediators like histamine

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50
Q

What percentage of WBCs do basophils constitute?

A

Basophils make up <0.5% of WBCs

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51
Q

What is the role of eosinophils?

A

Eosinophils are potent mediators that target extracellular parasites

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52
Q

When are eosinophils levels elevated?

A

Elevated levels, or eosinophilia, are seen in parasitic infections and allergies

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53
Q

What percentage of WBCs are monocytes?

A

Monocytes constitute 3-7% of WBCs

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54
Q

What do monocytes differentiate into?

A

Differentiate into macrophages in tissues

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55
Q

What are the functions of macrophages?

A

Macrophages perform phagocytosis, antigen presentation on MHC II, and cytokine secretion

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56
Q

What percentage of WBCs are lymphocytes

A

Lymphocytes make up 20-35% of WBCs

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57
Q

What are lymphocyte types?

A

B cells, T cells, and NK cells

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58
Q

What is the lifespan of circulating lymphocytes?

A

Lymphocytes circulate between blood and lymphoid tissues for about 4 months

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59
Q

What is the function of platelets?

A

Platelets are crucial for blood clotting

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60
Q

What is the role of red blood cells (RBCs)?

A

RBCs transport oxygen

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61
Q

Where do all blood cells originate?

A

Pluripotent stem cells in bone marrow

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62
Q

What are 3 lineages of blood cells?

A

Erythroid (RBCs, platelets), myeloid (monocytes, granulocytes), and lymphoid (B cells, T cells, NK cells)

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63
Q

How do granulocytes mature?

A

Granulocytes are released from the bone marrow as mature cells

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64
Q

Where do T cells mature?

A

Immature pre-T cells mature in the thymus

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65
Q

What happens to self-reactive T cells?

A

Self-reactive T cells are eliminated during development

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66
Q

Where do B cells mature in mammals?

A

B cells mature in bone marrow or Peyer’s patches, depending on the species

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67
Q

What is the role of NK cells, and where are they released from?

A

NK cells, part of innate immunity, are released mature from the bone marrow

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68
Q

What is the role of primary lymphoid tissues?

A

Primary lymphoid tissues are the sites of lymphocyte maturation

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69
Q

What are examples of primary lymphoid tissues?

A

Examples include the thymus (T cells), Bursa of Fabricius (birds), and bone marrow or Peyer’s patches (mammals)

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70
Q

What is the role of secondary lymphoid tissues?

A

Secondary lymphoid tissues are where mature lymphocytes encounter antigens

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71
Q

What are examples of secondary lymphoid tissues?

A

Examples include lymph nodes, spleen, and MALT (Mucosal Associated Lymphoid Tissue)

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72
Q

What do endothelial cells do during infection?

A

Endothelial cells upregulate adhesion molecules (“addressins”) to direct leukocytes to infection sites

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73
Q

What is the purpose of lymphatic circulation?

A

Lymphatic circulation allows lymphocytes to move between tissues and blood, increasing antigen encounter and immune response

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74
Q

What is inflammation?

A

A tissue reaction that delivers mediators of host defense to sites of infection or tissue damage

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75
Q

Inflammation - What are the primary roles in combating infection?

A
  1. Delivering effector molecules and cells to augment microbial killing
  2. Providing a physical barrier to prevent infection spread
  3. Promoting tissue repair
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76
Q

What is the main purpose of inflammation?

A

To focus the immune response at the site of infection or injury

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77
Q

What are the key steps in the acute inflammatory response?

A
  1. Production of cytokines and pro-inflammatory mediators in response to microbes or damaged cells
  2. Increased blood vessel permeability for plasma protein and leukocyte entry into tissues
  3. Destruction of microbes, clearance of damaged cells, and promotion of inflammation and repair
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78
Q

What are the cardinal signs of inflammation?

A

Pain, redness, heat, swelling, and loss of function

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79
Q

What causes pain?

A

Tissue destruction and irritation of sensory nerves

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80
Q

What causes redness?

A

Increased blood flow

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81
Q

What causes heat?

A

Increased blood flow and pyrogens

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82
Q

What causes swelling?

A

Fluid leakage and phagocyte infiltration

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83
Q

What causes loss of function?

A

When an entire tissue or organ is involved

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84
Q

What are the stages of neutrophil adhesion and emigration from blood vessels?

A

Neutrophils bind to vascular endothelial cells, adhere, and exit blood vessels to reach infection sites

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85
Q

What is Bovine Leukocyte Adhesion Deficiency (BLAD)?

A

BLAD is an autosomal recessive immunodeficiency in Holstein calves characterized by recurrent infections, oral ulcerations, chronic pneumonia, stunted growth, delayed wound healing, extreme neutrophilia, and inability of neutrophils to exit blood vessels due to an integrin gene mutation

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86
Q

Name three major pro-inflammatory cytokines :

A
  1. Tumor Necrosis Factor-α (TNF-α)
  2. Interleukin-1 (IL-1)
  3. Interleukin-6 (IL-6)
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87
Q

What are the functions of Tumor Necrosis Factor-α (TNF-α)?

A

Promotes inflammation, adhesion molecule expression, and fever

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88
Q

What are the functions of Interleukin-1 (IL-1)?

A

Induces fever, activates endothelial adhesion molecules, and promotes cell growth and repair

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89
Q

What are the functions of Interleukin-6 (IL-6)?

A

Triggers acute-phase protein production and systemic effects

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90
Q

What are the effects of IL-1, TNF-α, and IL-6 on the body?

A
  1. Low levels: Local inflammation (macrophage/endothelium activation).
  2. Moderate levels: Fever, lethargy, acute-phase protein production, neutrophilia.
  3. High levels: Vasodilation, vascular injury, DIC, ARDS, and septic shock.
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91
Q

What are chemokines, and give examples?

A

Chemokines are small cytokines that guide cell migration

Examples:

-CXCL8 (IL-8): Attracts and activates neutrophils

-CXCL2: Attracts neutrophils

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92
Q

What are the three types of vasoactive molecules?

A

Vasoactive amines, vasoactive peptides, and vasoactive lipids

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93
Q

What’s the function of vasoactive amines (e.g., histamine, serotonin)?

A

Increase vascular permeability

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94
Q

What’s the function of vasoactive peptides (e.g., C5a, bradykinin)?

A

Promote histamine release, pain, and vascular permeability

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95
Q

What’s the function of vasoactive lipids (e.g., prostaglandins, leukotrienes)?

A

Induce vasodilation, smooth muscle contraction, and chemotaxis

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96
Q

What is the function of histamine in inflammation?

A

Histamine, released by mast cells, causes vasodilation, increases vascular permeability, and stimulates nitric oxide production

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97
Q

How does the coagulation system function in inflammation?

A
  • Thrombin converts fibrinogen to fibrin, forming a physical barrier
  • The fibrinolytic system destroys fibrin, releasing peptides that attract neutrophils
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98
Q

What triggers the secretion of pro-inflammatory cytokines?

A

Sentinel cells activated by toll-like receptors (TLRs) and pattern-recognition receptors (PRRs) in response to PAMPs and DAMPs

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99
Q

Why are pro-inflammatory cytokines essential in low quantities but harmful in high quantities?

A

-Low quantities: Promote local inflammation and immune defense

-High quantities: Lead to systemic vasodilation, vascular injury, DIC, and ARDS

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100
Q

What is phagocytosis?

A

Phagocytosis is the ability of certain cells, called phagocytes, to ingest and destroy foreign particles. It literally means “eating by cells”

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101
Q

What are phagocytes?

A

Phagocytes are cells capable of ingesting and killing microorganisms that trigger an inflammatory response. Neutrophils and macrophages are examples of professional phagocytes

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102
Q

Which cells initiate the phagocytic process?

A

Neutrophils are the first to accumulate at the site of infection, followed by macrophages that migrate to the tissue to begin phagocytosis

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103
Q

What are the steps involved in phagocytosis?

A

The process includes:

  1. Chemotaxis: Movement of phagocytic cells to the site of infection
  2. Adherence: Phagocyte binds to the target particle
  3. Ingestion: Engulfment of the target
  4. Destruction: Intracellular killing and digestion of the target
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104
Q

What is opsonization?

A

The coating of bacteria with positively charged materials (opsonins) such as IgG, IgM, and C3b

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105
Q

How does opsonization aid phagocytosis?

A

Neutralizes the negative charge on bacteria, allowing neutrophils to adhere and engulf them

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106
Q

What are the receptors involved in neutrophil phagocytosis?

A

-Fc receptors: Bind antibodies (like IgG) attached to antigens

-C3b receptors: Bind C3b-coated bacteria for enhanced engulfment

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107
Q

What is a phagolysosome?

A

A phagolysosome is formed when the phagosome (containing the ingested microbe) fuses with lysosomes. This vesicle contains enzymes and toxic molecules that digest and kill the microbe

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108
Q

How are bacteria destroyed inside the phagolysosome?

A

Destruction occurs through:

  • Lytic enzymes and antimicrobial peptides
  • Oxidative metabolism (respiratory burst)
  • Neutrophil extracellular traps (NETs)
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109
Q

What are examples of lytic enzymes and peptides in neutrophil granules?

A
  • Primary granules: Hydrolases, lysozyme, defensins, and myeloperoxidase
  • Secondary granules: Lysozyme, lactoferrin, and collagenase
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110
Q

What is the oxygen-mediated killing mechanism?

A

It is the most potent neutrophil killing process, occurring in the phagolysosome and involving reactive oxygen species such as hypochlorite, hydrogen peroxide, and oxygen radicals

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111
Q

What is Chronic Granulomatous Disease?

A

It is a fatal condition caused by defective oxidative enzymes, impairing the respiratory burst pathway of neutrophils

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112
Q

What are neutrophils extracellular traps (NETs)?

A
  • NETs are extracellular meshes of nuclear material (DNA, histones) and granular proteins released by stimulated neutrophils to trap and kill bacteria
  • This active response is called NETosis
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113
Q

What happens to neutrophils after phagocytosis?

A

Neutrophils die and lyse after extended phagocytosis, forming pus

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114
Q

What is the role of macrophages after phagocytosis?

A

Macrophages egest debris, present microbial antigens to lymphocytes, and contribute to tissue healing by ingesting dead neutrophils

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115
Q

Which cells are the first responders to inflammation?

A

Neutrophils

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116
Q

What activates neutrophil migration to the infection site?

A

Cytokines activate vascular endothelial cells, facilitating neutrophil attachment and migration

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117
Q

What role do opsonins play in phagocytosis?

A

Opsonins like antibodies and complement enhance bacterial binding and ingestion by phagocytes

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118
Q

How are ingested microbes killed?

A

Through respiratory burst, antimicrobial peptides (e.g., defensins), and lytic enzymes

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119
Q

What is the lifespan of neutrophils?

A

Neutrophils are short-lived and cannot perform prolonged or multiple rounds of phagocytosis

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120
Q

What is the role of macrophages in chronic infections?

A

Macrophages eat surviving microbes, remove dying neutrophils, and initiate the healing process

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121
Q

How do macrophages support the adaptive immune system?

A

By presenting antigens to lymphocytes

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122
Q

What is the complement system?

A

The complement system is a group of serum and cell surface proteins activated by factors like antigen-antibody combinations. This activation leads to enzyme cascades with biological effects, including cell lysis and opsonization

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123
Q

What are the three pathways of complement activation?

A

Classical pathway, alternative pathway, and MB-Lectin pathway

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124
Q

What is the classical pathway?

A

Initiated by antibody-antigen binding (adaptive immunity)

125
Q

What is the alternative pathway?

A

Triggered by C3b binding to pathogen surfaces (innate immunity)

126
Q

What is the MB-Lectin pathway?

A

Activated by mannose-binding lectin binding to microbial carbohydrates (innate immunity)

127
Q

What are the key features of the classical pathway?

A
  • Initiated by antigen-antibody binding.
    Requires IgM or IgG antibodies
  • C1 protein binds to antigen-antibody complexes, activating the cascade

-The classical pathway forms a C3 convertase (C4b2b) which cleaves C3 into C3a and C3b

128
Q

How does the alternative pathway function?

A
  • Initiated when C3 spontaneously cleaves into C3a and C3b
  • C3b binds to pathogen surfaces
  • Factor B binds to C3b and is cleaved by Factor D, forming C3 convertase (C3bBb)
129
Q

How does the MB-Lectin pathway operate?

A
  • Mannose-binding lectin (MBL), a pattern recognition receptor (PRR), binds to mannose on microbial surfaces
  • Bound MBL activates MASP-2 (MBL-associated serine protease), which cleaves C4 and initiates the cascade
130
Q

What is the terminal complement pathway?

A
  • Common to all three pathways after C5 cleavage
  • Leads to the formation of the membrane attack complex (MAC), which punches holes in the microbial membrane, causing lysis and cell death
131
Q

What is the membrane attack complex (MAC)?

A
  • Formed by the sequential binding of complement components:
  • C5b binds C6, C7, C8, and multiple C9 molecules
  • C9 polymerizes to form a transmembrane pore
132
Q

What are the results of the membrane attack complex (MAC)?

A

Results in lysis of the target cell

133
Q

What regulates complement activation?

A
  • Factor H regulates the alternative pathway to prevent damage to host cells
  • Regulation occurs through substrate modulation to ensure proper targeting
134
Q

What are the key functions of the complement system?

A
  1. Opsonization
  2. Cell lysis
  3. Inflammation
  4. Immune clearance
135
Q

Define opsonization

A

C3b coats pathogens, enhancing phagocytosis

136
Q

Define cell lysis

A

MAC formation destroys microbial cells

137
Q

Define inflammation

A

C5a attracts immune cells and triggers inflammationD

138
Q

Define immune clearance

A

Removes immune complexes and dead cells

139
Q

What are the biological consequences of complement activation?

A
  • Enhanced phagocytosis through opsonization
  • Direct lysis of pathogens via MAC
  • Recruitment of immune cells through chemoattractants like C5a
140
Q

How do the complement pathways integrate innate and adaptive immunity?

A
  • Innate pathways (alternative and MB-lectin): Activated by microbial patterns (PAMPs)
  • Adaptive pathway (classical): Activated by antibodies bound to antigens
141
Q

What are cytokines?

A
  • Low molecular weight, secreted ‘messenger’ proteins
  • Regulate intensity and duration of innate and adaptive immune responses
  • Their activity is receptor-mediated
142
Q

What are the three main activities of cytokines?

A

Autocrine, paracrine, and endocrine

143
Q

What’s the function of autocrine?

A

Act on the cell that produced it

144
Q

What’s an example of autocrine?

A

IL-12

145
Q

What’s an example of paracrine?

A

IL-12

146
Q

What’s an example of endocrine?

A

IL-3, GM-CS

147
Q

What are some classifications of cytokines?

A
  • Monokines
  • Lymphokines
  • Interleukins
  • Interferons
  • Chemokines
  • Colony Stimulating Factors (CSF)
  • Growth Factors
148
Q

What produces monokines?

A

Monocytes

149
Q

What produces lymphokines?

A

Lymphocytes

150
Q

Define interleukins

A

Communication between leukocytes (e.g., IL-1, IL-2, IL-3)

151
Q

Define interferons

A

Inhibit viral replication

152
Q

Define chemokines

A

Attract specific cells to locations

153
Q

What do Colony Stimulating Factors (CSF) stimulate?

A

Stimulate stem cell differentiation in bone marrow

154
Q

What do Growth Factors stimulate?

A

Stimulate cell growth in vitro

155
Q

What are the three main categories of cytokine functions?

A
  1. Mediate and regulate innate immunity
  2. Mediate and regulate adaptive immunity
  3. Stimulate hematopoiesis
156
Q

What role do cytokines play in innate immunity?

A
  • Crucial in the first few days of infection.
  • Act immediately and may influence adaptive immune responses
157
Q

What are examples of cytokines that play in innate immunity?

A

IL-1, IL-6, TNFα, IL-12, and Type I interferons

158
Q

What are Type I interferons, and what do they do?

A
  • Includes IFNα and IFNβ
  • Produced by virally infected cells
  • Make other cells resistant to viral infection
159
Q

What is the role of Type II interferons (IFNγ)?

A
  • Functions in innate and adaptive immunity
  • Produced by NK cells and TH1 cells
  • Activates macrophages, neutrophils, and NK cells
  • Promotes TH1 development and suppresses TH2
  • Enhances B-cell IgG production
  • Upregulates MHC expression on APCs
160
Q

What are key roles of cytokines in adaptive immunity?

A
  • Produced primarily by T lymphocytes in response to antigen recognition
  • Regulate lymphocyte activation, growth, and differentiation
  • Enhance innate defenses
161
Q

Which cytokines regulate lymphocyte activation and growth?

A
  • IL-2: Lymphocyte proliferation.
  • IL-4 and IL-13: B-cell differentiation (IgE)
  • IL-10: Inhibits TH1
  • TGFβ: Treg cytokine, B-cell differentiation (IgA)
  • IFNγ: B-cell differentiation (IgG)
162
Q

Which cytokines enhance innate immunity?

A
  • IFNγ: Activates macrophages, neutrophils, and NK cells
  • TNF: Activates endothelial cells and neutrophils
  • IL-5: Activates eosinophils
163
Q

What is the role of cytokines in hematopoiesis?

A
  • Regulate growth and differentiation of bone marrow progenitor cells
  • Produced during innate and adaptive immune responses
164
Q

Name key hematopoietic cytokines:

A
  • Erythropoietin
  • Thrombopoietin & IL-11
  • IL-3
  • IL-5
  • GM-CSF
  • G-CSF
  • M-CSF
165
Q

What’s the function of erythropoietin?

A

Stimulates RBC production

166
Q

What’s the function of thrombopoietin & IL-11?

A

Stimulate platelet production

167
Q

What’s the function of IL-3?

A

Stimulates WBC production

168
Q

What’s the function of IL-5?

A

Eosinophil differentiation (e.g., during parasitic infection/allergy)

169
Q

What’s the function of GM-CSF?

A

Differentiation of neutrophils and monocytes

170
Q

What’s the function of G-CSF?

A

Differentiation of neutrophils

171
Q

What’s the function of M-CSF?

A

Differentiation of monocytes

172
Q

What mechanisms regulate cytokine activity?

A
  • Receptor antagonists
  • Soluble receptors
  • Opposing cytokines
  • Decoy receptors
173
Q

What’s the function of receptor antagonists?

A

Block cytokine receptors (e.g., IL-1 receptor antagonist)

174
Q

What’s the function of soluble receptors?

A

Neutralize cytokines (e.g., soluble TNF receptors)

175
Q

What type of effect do cytokines have?

A

Counteract effects (e.g., IL-4 vs. IFNγ for IgE)

176
Q

What’s the function of decoy receptors?

A

Bind cytokines without inducing signaling (e.g., decoy receptor for IL-1)

177
Q

What are five key concepts in cytokine signaling?

A
  1. Immune responses involve many cell interactions
  2. Cells communicate via cytokines and hormones
  3. Cytokines bind to specific target cell receptors
  4. Receptor binding activates transcription factors for gene expression
  5. Gene expression leads to new proteins and altered cell behavior
178
Q

What are some general properties of cytokines?

A
  • Secretion is brief and self-limited
  • Produced by diverse cell types
  • Act locally and/or systemically
  • Functions may overlap (redundancy)
  • Effects are synergistic and tightly regulated
179
Q

How does the innate immune system recognize pathogens?

A

Recognizes a limited number of conserved microbial PAMPs (Pathogen-Associated Molecular Patterns)

180
Q

What triggers the adaptive immune system?

A

Adaptive immunity can recognize and respond to almost all foreign macromolecules in invading microbes. These foreign molecules are called antigens

181
Q

What is antigenicity?

A

The inherent capacity of a molecule to be recognized by the immune system

182
Q

What are the two main types of antigens?

A

Microbial antigens and non-microbial antigens

183
Q

Give examples of microbial antigens:

A

Bacterial, viral, fungal, protozoan, arthropod, and helminth antigens

184
Q

Give examples of non-microbial antigens:

A

Food allergens, inhaled dust (pollen), blood-group antigens, histocompatibility antigens, and autoantigens

185
Q

What are autoantigens?

A

Antigens that induce autoimmune responses when the immune system attacks normal body components (e.g., thyroglobulin, myelin, mitochondrial proteins)

186
Q

What are examples of bacterial antigens?

A
  • Structural components: Peptidoglycans,
    lipoteichoic acid, lipopolysaccharides, pili, porins, and flagellar antigens (H)
  • Secreted products: Exotoxins, heat-shock proteins
  • Surface antigens: Capsular antigens (K)
187
Q

What are the key features of viral antigens?

A
  • A nucleic acid core surrounded by a protein capsid
  • Capsid: Made of capsomeres, which are highly antigenic
  • Viral proteins expressed on infected cells can provoke adaptive immunity
188
Q

What types of microbial antigens can trigger adaptive immunity?

A

Structural components of fungi, protozoan parasites, arthropods, and helminths

189
Q

Are all microbial antigens equally effective in triggering immunity?

A

No, their antigenicity varies, and adaptive responses may not always protect or eliminate the invader

190
Q

Food allergens

A

Can cause allergic reactions

191
Q

Pollens

A

Triggers immune responses when inhaled

192
Q

Blood-group antigens

A

Glycoproteins that can lead to immune reactions during mismatched transfusion

193
Q

Histocompatibility antigens

A

Involved in tissue graft rejection

194
Q

What factors influence antigenicity?

A
  • Size
  • Foreignness
  • Complexity
  • Stability
195
Q

Define size of antigenicity

A
  • Larger molecules are more antigenic
  • Molecules <1000 daltons are poor antigens
196
Q

Define foreignness of antigenicity

A

Greater structural difference from self-proteins increases immune response

197
Q

Define complexity of antigenicity

A

Complex structures (e.g., proteins) are more antigenic than simple ones (e.g., lipids)

198
Q

Define stability of antigenicity

A

Flexible or rapidly degraded molecules are poor antigens

199
Q

Why are proteins the best antigens?

A

They are large, complex, stable, and recognized well by the immune system

200
Q

Why are lipids and nucleic acids poor antigens?

A

Readily degradable, but nucleoproteins can be antigenic due to their protein carrier

201
Q

What are epitopes?

A
  • Specific regions on an antigen recognized by the immune system
  • A single large protein can have multiple epitopes
  • The most immunogenic epitopes are called immunodominant epitopes
202
Q

What is a hapten?

A

A small molecule (<1000 daltons) that is not antigenic alone but can become antigenic when attached to a larger carrier protein

203
Q

Examples of hapten

A
  • Penicillin allergy
  • Poison ivy
204
Q

Define penicillin allergy

A

Penicillin binds to proteins, forming an antigenic complex that triggers an allergic reaction

205
Q

Define poison ivy

A

Urushiol binds to skin proteins, resulting in allergic contact dermatitis

206
Q

What is cross-reactivity?

A

Identical or similar epitopes on unrelated molecules cause antibodies to react with both antigens

207
Q

Examples of cross-reactivity

A
  • Bacterial or food antigen mimics blood-group glycoproteins
  • Cross-reaction between Brucella abortus and Yersinia enterocolitica
  • FIP virus cross-reacting with pig transmissible gastroenteritis virus
208
Q

Define recognition

A

The adaptive immune system is optimized to recognize microbial macromolecules

209
Q

Define best antigens

A

Large, complex, stable, foreign proteins

210
Q

Define small molecules

A

Poor antigens unless linked to carriers (haptens)

211
Q

Define epitopes

A

Immune responses target specific areas of antigens

212
Q

What triggers adaptive immunity?

A

The capturing and presenting of foreign materials to cells that recognize them, performed by Antigen-Processing Cells (APCs)

213
Q

What are the three major types of Antigen-Processing Cells (APCs)?

A
  • Dendritic cells (DCs)
  • Macrophages
  • B-cells
214
Q

How do APCs initiate immune responses?

A

APCs capture foreign microbes or their products, process large proteins into peptides, and present them on their surfaces attached to Major Histocompatibility Complex (MHC) molecules

215
Q

Why are dendritic cells unique among APCs?

A

Only dendritic cells can activate naïve T cells and trigger a primary immune response

216
Q

Where are dendritic cells primarily found?

A

In epithelial tissues (skin, mucosa) and lymphoid organs (lymph nodes, spleen, thymus)

217
Q

What are the major functions of dendritic cells?

A
  • Serve as sentinel cells to activate innate defenses
  • Process exogenous antigens to initiate adaptive immunity
  • Regulate adaptive immunity
218
Q

What makes dendritic cells highly efficient APCs?

A

They express 100 times more MHC II molecules than any other APC and can activate up to 3000 T-cells per activated dendritic cell

219
Q

How do follicular dendritic cells (FDCs) differ from other dendritic cells?

A
  1. Do not migrate
  2. Are located in lymphoid follicles (B-cell areas)
  3. Lack MHC II molecules on their surface
  4. Carry many complement and Fc receptors
220
Q

What is the primary function of follicular dendritic cells (FDCs)?

A

To present antigens to B-cells without processing them

221
Q

What are iccosomes?

A

Spherical bodies on FDC dendrites formed from antigen:antibody complexes, which are ingested by activated B-cells

222
Q

How do dendritic cells capture antigens in tissues?

A

By constantly sampling extracellular fluid through macropinocytosis

223
Q

What triggers dendritic cells to migrate to lymph nodes?

A

The inflammatory cytokine TNF-⍺ during infection

224
Q

What happens as dendritic cells migrate to lymph nodes?

A

They upregulate expression of MHC II molecules and co-stimulatory molecule B7, ensuring effective antigen presentation

225
Q

Why are macrophages less efficient APCs than dendritic cells?

A

They express lower levels of MHC II and co-stimulatory molecules unless activated by cytokines like INFγ

226
Q

What role do B-cells play in antigen presentation?

A

B-cells present antigens to T-helper cells during the secondary immune response and become efficient APCs after activation

227
Q

What changes occur in B-cells after activation?

A

They upregulate MHC II and co-stimulatory B7 molecule expression, becoming potent activators of T-helper cells

228
Q

What is required for an antigen to trigger an adaptive immune response?

A

Antigen molecules must be broken into fragments, bound to MHC molecules, and presented to T-cells

229
Q

What are MHC molecules, and how are they encoded?

A

MHC molecules are glycoproteins encoded by a gene cluster called the major histocompatibility complex (MHC)

230
Q

What is the function of MHC molecules in immunity?

A

MHC molecules control antigen presentation and influence susceptibility to infectious and autoimmune diseases

231
Q

What are the three classes of MHC gene loci?

A

Class I, II, and III

232
Q

What does class I encode?

A

Encodes MHC I molecules, present on all nucleated cells

233
Q

What does class II encode?

A

Encodes MHC II molecules, restricted to professional APCs

234
Q

What does class III encode?

A

Encodes proteins like complement proteins involved in innate immunity

235
Q

How do MHC I and MHC II molecules differ in distribution and function?

A
  • MHC I: Found on most nucleated cells; presents antigens to cytotoxic T cells, resulting in T-cell-mediated toxicity
  • MHC II: Found on B cells, macrophages, and dendritic cells; presents antigens to T-helper cells, resulting in T-cell-mediated help
236
Q

How are MHC molecules named in different species?

A
  • Humans: HLA
  • Dogs: DLA
  • Cattle: BoLA
  • Horses: ELA
  • Pigs: SLA
237
Q

What are the subtypes of MHC I molecules?

A

MHC Ia, Ib, Ic, and Id

238
Q

Define MHC Ia

A

Polymorphic, expressed on most nucleated cells

239
Q

Define MHC Ib

A

Reduced expression, limited ligand binding

240
Q

Define MHC Ic

A

nvolved in NK cell signaling

241
Q

Define MHC Id

A

Binds PAMPs (pathogen-associated molecular patterns)

242
Q

What is the structure of an MHC Ia molecule?

A
  • Composed of a heavy α chain and a β2-microglobulin chain
  • The α chain forms the antigen-binding groove, while β2-microglobulin stabilizes the structure
243
Q

How are peptides bound to MHC I molecules?

A

Peptides are 8-10 amino acids long, anchored at both ends, and fit within the binding groove

244
Q

What is the endogenous pathway of MHC I?

A

Proteins manufactured within the cell are processed into peptides, bound to MHC I molecules, and presented on the cell surface for CD8+ T-cell recognition

245
Q

Where are MHC II molecules found, and what is their structure?

A

Found on professional APCs, consisting of an α chain and a β chain, with their peptide-binding groove formed by the α1 and β1 domains

246
Q

How do peptides bind to MHC II molecules?

A

Peptides are 13-20 amino acids long, with part of the peptide protruding from the groove

247
Q

What is the exogenous pathway of MHC II?

A

Antigens are internalized, processed, and bound to MHC II molecules in vesicles. These complexes are transported to the cell surface for presentation to CD4+ T cells

248
Q

What is encoded by MHC Class III genes?

A

Complement proteins and other molecules important for innate immunity

249
Q

What is MHC restriction?

A

Only antigen fragments bound to MHC molecules can trigger an adaptive immune response

250
Q

How does MHC expression affect disease susceptibility?

A
  • Specific MHC alleles determine susceptibility or resistance to diseases
  • Heterozygotes benefit from responding to a broader range of antigens
251
Q

Give examples of MHC-associated disease resistance or susceptibility

A
  • BoLA-Aw7: Resistance to bovine leukosis
  • BoLA-A*16: Resistance to mastitis
  • ELA-A9: Susceptibility to equine recurrent uveitis
252
Q

What is the role of lymphocytes in the immune system?

A

Lymphocytes are central to the adaptive immune system and body defenses

253
Q

What are the three major types of lymphocytes?

A

B cells, T cells, and natural killer (NK) cells

254
Q

What’s the functions of B cells?

A

Responsible for antibody production

255
Q

What’s the functions of T cells?

A

Regulate adaptive immunity and are responsible for cell-mediated immune responses

256
Q

What’s the functions of natural killer (NK) cells?

A

Play a role in innate immunity

257
Q

What is unique about lymphocyte subpopulations?

A

Within the major types, there are many subpopulations with different characteristics and functions

258
Q

What are the structural characteristics of lymphocytes?

A
  • Small, round cells, 7-15 μm in diameter
  • Large, round nucleus that stains intensely with hematoxylin
  • Thin rim of cytoplasm containing mitochondria, free ribosomes, and a small Golgi apparatus
259
Q

How do NK cells differ structurally from T and B cells?

A

NK cells are usually larger and may contain obvious cytoplasmic granules

260
Q

Can the structure of a lymphocyte indicate its function?

A

No, except for NK cells with granules, lymphocyte structure does not provide clues to their function

261
Q

Identify features of B cells in the development site

A

Bone marrow, bursa, Peyer’s patches

262
Q

Identify features of B cells in the distrubition

A

Lymph node cortex, splenic follicles

263
Q

Identify features of B cells in the antigen receptors

A

BCR (immunoglobulin)

264
Q

Identify features of B cells of important surface antigens

A

Immunoglobulin

265
Q

Identify features of B cells of antigen recognized

A

Free foreign proteins

266
Q

Identify features of B cells of progeny cells

A

Plasma cells, memory cells

267
Q

Identify features of B cells of secreted products

A

Immunoglobulins

268
Q

Identify features of T cells in development site

A

Thymus

269
Q

Identify features of T cells in distribution

A

Lymph node paracortex, splenic periarteriolar sheathI

270
Q

Identify features of T cells in antigen receptors

A

TCR (protein heterodimer) associated with CD3, CD4, or CD8

271
Q

Identify features of T cells of important surface antigens

A

CD2, CD3, CD4, or CD8

272
Q

Identify features of T cells in antigen recognized

A

Processed foreign proteins in MHC

273
Q

Identify features of T cells in progeny cells

A

Effector T cells, memory T cells

274
Q

Identify features of T cells in secreted products

A

Cytokines

275
Q

What is the overview of lymphocyte maturation?

A

Lymphocytes mature through stages involving antigen receptor development and selection processes to ensure proper immune response

276
Q

How are T and B cells segregated in peripheral lymphoid organs?

A
  • T and B cells occupy distinct regions:
  • T cells: Paracortex of lymph nodes and periarteriolar sheath of the spleen
  • B cells: Cortex of lymph nodes and splenic follicles
277
Q

What are the two main T cell receptor types, and how are they categorized?

A
  • Alpha-beta (αβ) T cells: Includes CD4+ and CD8+ T cells
  • Gamma-delta (γδ) T cells: Defined by their unique TCR, important at mucosal surfaces
278
Q

What are the subtypes of CD4+ αβ T cells?

A

TH 1, TH2, TH17, and Treg

279
Q

What’s the function of T helper 1 (TH1)?

A

Secretes IFNγ, IL-2; activates phagocytes, NK cells, CTLs; defends against intracellular pathogens

280
Q

What’s the function of T helper 2 (TH2)?

A

Secretes IL-4, IL-5, IL-9, IL-13; activates mast cells, eosinophils, and B cells for IgE production

281
Q

What’s the function of T helper 17 (TH17)?

A

Secretes IL-17, IL-21, IL-22; attracts neutrophils and monocytes, induces acute inflammation

282
Q

What’s the function of T regulatory (Treg)?

A

Secretes IL-10, IL-35, TGFβ; suppresses T cell responses, prevents self-reactive immune reactions

283
Q

What is the role of CD8+ αβ T cells?

A

CD8+ T cells (Cytotoxic T Lymphocytes) recognize antigens on MHC I, clonally expand, and kill cells expressing foreign antigens

284
Q

How do γδ T cells differ from αβ T cells?

A

γδ T cells recognize unprocessed antigens, including stress proteins, and are prominent at mucosal surfaces

285
Q

What are the unique features of NK cells?

A
  • Large granular lymphocytes
  • Part of innate immunity, not antigen-specific.
  • Lack surface immunoglobulins, CD3, CD4, or CD8
  • Activated by IFNγ, TNF, and IL-2
286
Q

What is the cytotoxic role of NK cells?

A

NK cells target cells lacking normal MHC I or expressing stress proteins

287
Q

What are the three major receptors of NK cells?

A

NK cells use receptors to detect abnormal surface antigens, including stress markers

288
Q

What is the structure of the T cell receptor (TCR) complex?

A
  • TCR consists of paired peptide chains (αβ or γδ) that form antigen-binding receptors
  • It connects to a signal-transducing component called CD3
289
Q

How can you tell if a T cell is a T helper cell by its structure?

A
  • A T cell with TCR/CD3 associated with CD4 is a T helper cell
  • CD4 binds to MHC class II molecules on antigen-presenting cells (APCs)
290
Q

What is the role of CD4 and CD8 in T cells?

A
  • CD4: Binds to MHC class II molecules on APCs, identifying T helper cells
  • CD8: Binds to MHC class I molecules on all nucleated cells, identifying cytotoxic T cells
291
Q

What are the key interactions in a T cell-APC dialog?

A
  • TCR binds to antigenic peptides linked to MHC molecules
  • Co-stimulation signals (e.g., cytokines) are required for full activation
292
Q

What is an immunological synapse?

A
  • It’s the interaction site between a T cell and an APC
  • SMACs (Supramolecular Activation Clusters) form concentric rings:
  • cSMAC: Central region for signaling
  • pSMAC: Peripheral region for adhesion
293
Q

What happens if co-stimulation signals are absent?

A

The T cell fails to activate properly, and the immune response is terminated

294
Q

What are T helper cells, and how do they function?

A
  • CD4+ T cells recognizing antigens displayed on MHC II molecules
  • They are categorized by the cytokines they secrete, not surface molecules
295
Q

What are the main types of T helper cells?

A
  • TH1: Promote cell-mediated immunity
  • TH2: Support antibody production
  • TH17: Enhance neutrophil-mediated inflammation
  • Treg: Suppress immune overactivation
296
Q

How do naïve T helper cells differentiate into subsets?

A
  • Differentiation depends on signals received from APCs and the local environment
  • Stimulating cytokines determine the subset:
  • TH1: IL-12
  • TH2: IL-4
  • TH17: IL-6, TGF-β, and IL-23
297
Q

How do TH subsets regulate each other?

A

Each subset produces cytokines that amplify its own function while inhibiting others

298
Q

What cytokines do TH1 cells secrete, and what are their functions?

A
  • Cytokines: IFN-γ, IL-2
  • Functions: Activate macrophages, NK cells, cytotoxic T cells, and B cells
299
Q

What cytokines do TH2 cells secrete, and what are their functions?

A
  • Cytokines: IL-4, IL-5, IL-13
  • Functions: Stimulate IgE production, mast cell activation, and eosinophil recruitment
300
Q

What cytokines do TH17 cells secrete, and what are their functions?

A
  • Cytokines: IL-17, IL-21, IL-22
  • Functions: Promote inflammation and defense against extracellular bacteria and fungi
301
Q

What are the functions of T regulatory (Treg) cells?

A

Secrete IL-10, IL-35, and TGF-β to suppress immune responses and maintain self-tolerance

302
Q

What are γδ T cells, and where are they found?

A

T cells with γδ receptors, often found in intestinal walls (humans) or circulating in ruminants and pigs

303
Q

What is the role of γδ T cells?

A
  • Recognize unprocessed antigens and stress proteins
  • Act in innate immunity at mucosal surface
304
Q

What are the key characteristics of TCR and antigen recognition?

A
  • TCR binds peptides linked to MHC molecules on APCs
  • Co-stimulation is required for activation
305
Q

TH1 characteristics

A

Stimulating cytokines: IL-12
Secreted cytokines: IFN-γ, IL-2
Function: promotes cell-mediated immunity

306
Q

TH2 characteristics

A

Stimulating cytokines: IL-4
Secreted cytokines: IL-4, IL-5, IL-13
Function: supports antibody production (e.g., IgE)

307
Q

TH17 characteristics

A

Stimulating cytokines: IL-6, TGF-β, IL-23
Secreted cytokines: IL-17, IL-21, IL-22
Function: stimulates neutrophil responses

308
Q

Treg characteristics

A

Stimulating cytokines: IL-10, TGF-β
Secreted cytokines: IL-10, IL-35, TGF-β
Function: suppresses immune overactivation

Immunology (1 decks)

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