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NRS 250: Exam 1 > Module 10: The Immune System > Flashcards

Module 10: The Immune System Flashcards

1
Q

Where does lymph return to the blood

A

via the left and right subclavian veins

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2
Q

Lymph Nodes: Definition and Function

A
  • highly organized small organs less than 1inch in length
  • optimize pathogen and lymphocyte interactions
  • they are concentrated regions of B-cells and T-cells
  • become swollen with infection when lymphocytes proliferate
  • Function:
    • filtration: macrophages to clean up debris
    • i_mmune activation_: lymphocytes to search for pathogens and infection
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3
Q

Tonsils: Location and Function

A
  • 5 total:
    • pharyngeal tonsils: posterior wall of the nasopharynx
    • palatine tonsils: boundary between soft palate and pharynx
    • lingual tonsil: base of the tongue
  • Function:
    • contain lymphocytes that destroy and remove pathogens that enter through air and food
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4
Q

Appendix: Location and Function

A
  • Location:
    • at the beginning of the large intestine
  • Function:
    • contains high concentration of lymphoid follicles
    • protect against harmful bacteria in intestines
    • lymphocyte source for intestines
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5
Q

Spleen: Location and Function

A
  • blood-rich, soft organ in the LUQ
  • Function:
    • contains lymphocytes that initiate immune responses to antigens in the blood (blood borne pathogens)
    • removes debris and old blood cells and platelets from the blood
    • stores RBC breakdown products
    • stores platelets and WBCs
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6
Q

Thymus: Location and Function

A
  • Location:
    • bilobed developmentally regulated organ in the mediastinum
  • Function:
    • matureation of T-lymphocytes
    • most active during childjood, it stops growing during adolescence and then gradually atrophies
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7
Q

Innate Immunity: Definition and the Natural Barriers

A
  • Definition:
    • composed of natural barriers to pathogen invasion and a general inflammatory response that prevents further infection and promotes healing
  • Natural Barriers:
    • physical
      • epithelial cells of the skin and external surfaces
        • frequent turnover to replace dead cells and remove bacteria
    • biochemical
      • secretions meant to trap or destroy microorganisms
        • ex: mucus, perspiration, saliva, tears, earwax
      • Antimicrobial molecules:
        • small peptides secreted by epithelia cells and found in granules of leukocytes that disrupt cell membrane of bacteria
          • ex. cathelicidins, defensins
    • microbiome
      • good bacteria that compete with bad bacteria for nutrients and block pathogen adherence
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8
Q

Pathogen: Definition and Examples

A
  • A pathogen is a disease producing micro-organism such as:
    • bacteria: living, single-celled microorganism that can reproduce or grow on their own
    • viruses: non-living DNA or RNA wrapped in protein that takes over host cells to reproduce
    • fungi: living, single or multicellular organisms
    • parasites: large group of the creppy crawlies!
    • prions: proteins gone bad…
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9
Q

Antigen: Definition

A
  • antigens are any molecule or partial molecule from a pathogen
    • cell proteins, carbohydrates, lipids that are part of bacterial cell structure
    • bacterial released toxins
    • other large, complex “non-self” molecules
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10
Q

Immunogen: Definition

A
  • an antigen that invokes an immune response
    • ex. cell proteins and toxins = excellent immunogens
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11
Q

Inflammation Definition and Cardinal Signs

A
  • inflammation is a cascade of events intitated when body tissues are damaged
  • Cardinal Signs
    • ​Redness
    • Heat
    • Swelling
    • Pain
    • visible within seconds of injury
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12
Q

Vascular Changes with Inflammation

A
  • vasodilation that causes increased permeability
    • deliver leukocytes, plasma proteins, and biochemical mediators to site of injury
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13
Q

Migration to Tissue Injury Site in Inflammation

A
  • migration: cells attracted to site of injury due to inflammatory mediators
  • margination: cells move along the wall of the blood vessel
  • diapedesis: cells pass through the blood vessel walls to injured tissue
  • phagocytosis: cells engulf pathogens and debris at site of injury
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14
Q

Diapedesis

A

diapedesis: cells pass through the blood vessel walls to injured tissue

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15
Q

Tissue Response and Inflammation

A
  • tissues responses to mediators and cellular changes:
    • to prevent infection:
      • dilution of toxins
      • activation of plasma protein systems
      • phagocytosis of pathogens and debris
    • to prevent spread:
      • clotting system activation
    • activate adaptive immune reponse
    • begin the healing process
      • removal of dead cells, products via lymph, etc.
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16
Q

Purulent Exudate

A
  • exudate = “pus”
  • fluid at site of injury with white blood cells, proteins, microbial debris, and cellular debris
  • this is a sign of infection
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17
Q

Transudate

A
  • clear fluid at site of injury which is mainly water filtrate from the blood
  • less likely to be infected
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18
Q

3 Plasma Protein Systems in Inflammation

A
  1. Complement system
    1. classic pathway
    2. lectine pathway
    3. alternative pathway
  2. Clotting System
  3. Kinin System
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19
Q

Plasma Protein Systems: The Complement System

A
  • Activated by 3 general mechanisms:
      1. Classic Pathway
      1. Lectin Pathway
      1. Alternative Pathway
  • it is a cascade of molecules released that have many functions in the immune system
    • 30 plasma proteins (C1-C9…), made by hepatocytes in the liver, and immune cells
    • “complement” or enhances phagocytic and antibody responses
  • Attracts Phagocytes: through production of opsonins and chemotaxins
  • Increases Inflammation:
    • some of the C proteins are anaphylatoxins
      • they cause Mast Cells and Basophils to degranulate→release of histamines → INFLAMMATION
        • increased vascular permability
        • smooth muscle contraction
        • bronchoconstriction
  • Forms the Membrane Attack Complex: destroys pathogen directly by putting a large channel in the membrane of the pathogen that disrupts osmotic balance and causes the cell to swell and burst
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20
Q

Membrane Attack Complex

A
  • formed in the complement system of plasma protein system
  • Membrane Attack Complex: destroys pathogen directly by putting a large channel in the membrane of the pathogen that disrupts osmotic balance and causes the cell to swell and burst
    • pathogen lysis
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21
Q

Complement System Activation

A
  1. Classic Pathway: activated by antigen-antibody complex
  2. Lectin Pathway: activated by lectins binding to specific sugars (mannose) on the surface of the beacterium
  3. Alternative Pathway: activated by bacterial surface polysaccharides, etc.
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22
Q

Plasma Protein Systems: The Clotting System

A
  • aka Coagulation
  • proteins that form a fibrin meshwork at injury site
  • stops bleeding
  • prevents spread of infection
  • traps microorganisms for removal
  • framework for repair and healing
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23
Q

Plasma Protein Systems: the Kinin System

A
  • group of proteins, including bradykinin
    • activated by factor XIIa from the clotting cascade
  • cause:
    • dilation of blood vessels
    • stimulate nerve endings (pain)
    • smooth muscle contraction
    • increased permeability and leukocytosis
    • limited by kininases that degrade these proteins very rapidly
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24
Q

Interferons

A
  • anti-viral proteins that help cells non-specifically target and prevent viral replication
    • released in response to detection of viral nucleic acids
    • reeleased from any body cell infected by a virus
    • triggers virus-blocking enzyme release in body cells that breakdown viral mRNA
      • this inhibits viral protein synthesis
  • activate the immune system
  • slow cell division and tumor growth in body cells
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25
Q

Functions of Inflammatory Cells (examples)

A
  • recognize a limited range of pathogens or pathogen related molecules
  • secrete inflammatory mediators
    • cytokines:
      • interleukins
      • interferon
      • tumor necrosis factor -alpha
    • chemockins
  • kill pathogens and remove debris
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26
Q

Circulating Inflammatory Cells

A
  1. neutrophils
  2. monocytes
  3. eosinophils
  4. lymphocytes
  5. basophils
  6. platelets
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27
Q

Connective Tissue Inflammatory Cells

A
  1. mast cells
  2. fibroblasts
  3. macrophages
  4. lymphocytes
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28
Q

Neutrophil

A
  • white blood cell
  • short lived: 6-12 hours
  • pus
  • phagocytosis
  • lobed nucleus
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29
Q

Eosinophil

A
  • white blood cell
  • parasite response
  • regulate inflammatory mediators by degrading vasoactive molecules
  • degrade histamine
30
Q

Basophils

A
  • white blood cell
  • allergies
  • asthma
  • similar to mast cells
  • basophilic granules
31
Q

Monocytes

A
  • white blood cell
  • immature phagocytes
    • become phagocytes through maturation
32
Q

Mast Cell

A
  • type of connective tissue inflammatory cell
  • NOT basophils but look similar, have a different precursor origin
  • Function:
    • found in vascularized connective tissues, near epithelium (dermis, GI tract, respiratory tract)
    • **INFLAMMATION**
    • increased permeability of blood vessels
    • smooth muscle contraction
    • regulation of other cells during inflammation and healing by release and synthesis of inflammatory mediators
      • histamine
      • tryptase
      • cytokines, prostaglandins, lekotrienes, growth factors
33
Q

Mast Cells are activated by:

A
  • physical injury: heat, trauma, UV light, radiation
  • chemical agents: toxins, venom, proteolytic enzyme, antimicrobial peptides
  • immunologic activation: anaphylatoxins, IgE, bacteria, viruses
34
Q

Mast Cell Degranulation

A
  • release of contents within granules
    • chemotactic factors: attract leukocytes, espc. neutrophils
    • MOSTLY RELEASE HISTAMINES
      • proinflammatory (H1) receptors
        • smooth muscle of bronchi causes bronchoconstriction
      • anti-inflammatory (H2) receptors)
        • secretion of gastric acid from parietal cells
35
Q

Injury to endothelium and subendothelial connective tissue triggers:

A
  • endothelial cells
    • adherence of leukocytes
    • migration of leukocytes to tissue
    • prothrombotic events: platelet activation, clot formation
  • Platelets:
    • hemostasis, coagulation cascade
    • release granules: inflammatory mediatorys, coagulation, growth factors, adhesion molecules, protease inhibitors, Calcium, magnesium
    • serotonin–vascular effects similar to histamine
36
Q

Phagocytes

A
  • Neutrophils and monocytes/macrophages are primary phagocytes for destruction of bacteria
    • neutrophils = first response
    • macrophages and others come later
  • Phagocytosis:
    1. recognition and adhesion of bacteria
      1. they have antigens that are recognized
    2. engulf: forms phagosome
    3. lysosome fuses with the phagosome and forms phagolysosome
    4. destruction and digestion
37
Q

Natural Killer Cells

A
  • CD16 and CD25
  • specialized to nonspecifically detect and destroy virus infected cells and tumor cells
    • detect “non-self” by looking for cells low in MHC “self” markers
  • release cells called perforins that lyse the cell membranes of targets
  • activated by cytokines
  • important alternative to B and Tcell mediated immunity
  • **these responses are conserved across species**
38
Q

Regeneration

A
  • a process where damaged tissue is replaced with healthy tissue of the original type
39
Q

Repair

A
  • replacement of destroyed tissue with scar tissue
  • not as good as regeneration
40
Q

Scar Tissue

A
  • composed primarily of collagen, a substance which fills in the lesion and restores tissue integrity and strength, but cannot carry out the physiological functions of of the tissue it has replaced
    • **Results in a loss of function**
41
Q

Primary Intention

A
  • wounds that have minimal tissue loss, such as papercuts or surgical incisions
    • require very little sealing (epithelialization) and shrinkage (contraction)
  • faster process than secondary intention
  • heals primarily through the process of collagen synthesis
42
Q

Secondary Intention

A
  • much slower than primary intention
  • requires a lot of tissue replacement
    • this causes epithelialization, scar formation, and contraction to take longer
43
Q

Phases of Wound Healing

A
  1. Phase 1: hemostasis
    1. takes seconds to hours
      1. vasoconstriction
      2. platelet aggregation
      3. leucocyte migration
  2. Phase 2: Inflammatory Phase
    1. takes hours to days (1-3 days)
      1. early–neutrophils
      2. chemoattractant release
      3. late macrophages
      4. phagocytosis and removal of foreign body/bacteria
  3. Phase 3: Proliferative Phase
    1. takes days to weeks (3 days to 1 month)
      1. fibroblast proliferation
      2. collagen synthesis
      3. ECM (extracellular matrix) reorganization
      4. angiogenisis
      5. epithelialization
  4. Phase 4: Remodeling
    1. takes weeks to months
      1. remodeling
      2. epithelialization
      3. ECM remodeling
      4. increase in tensile strength of wound
44
Q

Causes of Dysfunctional Wound Healing

A
  • ischemia
  • excessive bleeding
  • excessive fibrin deposition
  • predisposing disorder i.e. diabetes mellitus
  • obesity
  • wound infection
  • inadequate nutrition
  • use of certain drugs
  • **tobacoo smoking**
45
Q

Examples of Dysfunctional Wound Healing

A
  • chronic wounds: last a long time
  • wound disruption: wound continually sloughs off
  • dehiscence: sutured wound pulls apart
  • contracture: excessive wound contraction may result in deformity
46
Q

B-Cells

A

B-Lymphocytes

  • born AND mature in the bone marrow
  • activated by CD4-T-Cells
  • housed in lymphoid tissues
  • recognize free pathogens (bacteria, toxins, viruses)
  • involved in antibody-mediated immunity (aka Humoral Immunity)
  • have specific antigen receptors: B-Cell Receptors (BCRs)
47
Q

T-Cells

A

T-Lymphocytes

  • born in bone marrow, mature in Thymus
  • housed in lymphoid tissues
  • recognize infected or cancerous body cells
  • involved in cell-mediated immunity
  • involved in activating total, combined immune responses
  • have specific antigen receptors:
    • T-cell Receptors (TCRs)
48
Q

The adaptive immune system is:

A

Humoral (antibody mediated) Immunity and Cellular (Cell-Mediated) Immunity

  • antigen-specific: requires the production of specific lymphocytes and antibodies against a specific antigen
  • systemic: not restricted to the initial infection site
  • has memory: second encounter causes a more rapid and vigorous response
49
Q

Antibody

A
  • aka immunoglobin
  • Y -shaped protein made by plasma cells in response to a SPECIFIC antigen
  • each antibody can only bind to **one specific antigen**
    • the purpose of this binding is to help destroy the antigen
  • an antibody is a type of immunoglobulin
50
Q

Immunocompetent Cells

A

B cells or T Cells

  • cells display a unique type of receptor that responds to a distinct antigen
    • become immuncompetent before they encounter antigens they may later attack
    • are exported to secondary lymphoid tissue where encounters with antigens occur
    • mature into fully functional antigen-activated cells upon binding with their recognized antigen
51
Q

Lymphocyte Development

A
  • origin: bone marrow, hematopoietic stem cells
  • maturation: bone marrow (B cells) or thymus (T cells)
  • immunocompetence: able to recognize one specific antigen, displays unique antigen receptor
  • **Self-Tolerance**: able to recognize “self” cells and be unresponsive to self-antigens
    • positive selection: maintain only cells that recognize “self” proteins -MHC
    • negative selection: remove cells that are reactive to “self”- self-antigen
52
Q

Lymphocyte Activation

A
  • activation: happens when they actually encounter their specific antigen in the body
  • proliferation and differentiation: once activated they will increase in number and make other immune cells
53
Q

B-Cell Activation

A

Humoral (antigen-mediated) Immunity

  1. Pathogen invades the body
  2. B-cells with BCRs (B-Cell Receptors) are waiting to find their specific antigen
  3. Specific B-Cells with BCR recognizes specific pathogen and makes
    1. plasma cells: produce specific antibodies for that pathogen
      1. 2000 antibodies per second
      2. lifespan of 5-7days
    2. memory cells: store memory of antigens to produce antibodies upon later infection, lay dormant until 2nd infection by same organism
54
Q

IgG

A
  • MOST COMMON
  • secreted to respond to most antigens
  • highest after second exposure
  • memory
  • crosses placenta
  • small monomer
55
Q

IgM

A
  • primary reaction
  • stays on B-cell to act as B-cell receptor for antigen
  • pentamer with 10 antigen binding sites
56
Q

IgA

A
  • secreted mostly in:
    • mucus membranes
    • tears
    • saliva
    • nasal
    • respiratory
    • gastrointestinal
    • breast milk
  • dimer with 4 binding sites
57
Q

IgE

A
  • secreted to respond to parasitic worms, allergic responses
  • larger monomer
58
Q

IgD

A
  • binds to basophils and mast cells during hypersensitivity reactions
  • small monomer
59
Q

Anatomy of a an Antibody

A
60
Q

Antibody-Mediated Responses

A
  1. Neutralize: combine with molecules, viruses to physically prevent them from interacting with cells
  2. agglutination: clump molecules, bacterial cells together, render non-functional
  3. Precipitation: separate them from solution like a chemical precipitate
  4. Tagging for Destruction: mark free pathogens, attract other cells to destroy them
    1. complement system
    2. phagocytes
    3. natural killer cells
61
Q

Active Immunity vs. Passive Immunity

A
  • Active Immunity: occurs when antibodies are made actively by memory cells
    • present as long as memory cells are intact
      • natural: due to infection with pathogen
      • artificial: vaccines with attenuated pathogens
  • Passive Immunity: occurs when antibodies are put into the body without memory cells, gone when supply is gone
    • natural: breastmilk, IgA
    • artificial: serum injection
62
Q

Self Cells vs Infected Cells

A
  • “self” is signified by MHC proteins on cell surface
  • antigen presenting cells will display antigens from phagocytized pathogens
63
Q

3 Types of T-Cells

A
  1. cytotoxic T-Cells (CD8)
  2. helper T-Cells (CD4)
  3. Regulatory T-Cells (CD4-25)
64
Q

Class I MHC - SELF

A
  • “MHC-self” signals that it is a self cell
  • present on every body cell like a biochemical fingerprint, varies across individuals
  • can display antigens “MHC I-antigen” signals that it is a body cell that has been infected
65
Q

Class II MHC- APC

A
  • present only on antigen presenting cells
  • “MHCII-antigen” complex signals that an invading pathogen has been found by an APC
66
Q

Cytotoxic T-Cell Function

A
  • aka CD8 cells
  • recognize body cells infected by pathogens by binding to MHC 1-self-antigen complexes
  • CD8 cells then destroy infected body cells by lysis or granzymes/perforin released from its granules that induce apoptosis
    • can be:
      • virus infected
      • mutated cancer cells
      • transplanted donor cells
67
Q

Helper T-Cells

A
  • aka CD4 cells
  • recognize APC MHC II-antigen presenting cells
  • release cytokines, chemicals that are necessary to activate other immune cells
    • activate B-cells
    • activate cytotoxic T-cells
    • attract neutrophils and macrophages
68
Q

Regulatory T-Cells

A
  • aka CD4-25
  • inhibit innate and adaptive immune responses to keep the system in check
  • under research for autoimmune disease control
69
Q

Helper T-Cells (CD4) activate B Cells

A
  • helper T-Cells (CD4) stimulate and activate B-Cells
  • Helper T-Cells can also recognize APC MHC II- antigen on B-cells
  • release immune stimulating molecules to activate B-cells
  • required for complete B-cell response
  • **HIV virus attacks Helper T-cells**
70
Q

opsonin

A

released by the complement system

attracts phagocytes and helps them to phagocytize pathogens

71
Q

defensins

A

small peptides secreted by eptihelia cells and found in granules of leukocytes (neutrophils) that distrupt cell membrane of bacteria

72
Q

DAMPs and PAMPs

A
  • Damage associated Molecule Patterns:
    • released when membranes are damaged or cells die
  • Pathogen Associated Molecule Patterns:
    • conserved patterns across pathogens
      • peptidoglycans
      • lipopolysaccharides
      • viral RNA/DNA
  • detected by PRRs
    • pattern recognition receptors
    • located on leukocytes
      • natural killer cells
      • mast cells

NRS 250: Exam 1 (11 decks)

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