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PHYS 261 > Chapter 24 > Flashcards

Chapter 24 Flashcards

1
Q

3 functions of Immunity

A

1 recognize/remove abnormal self cells
2 removal of dead/damaged cells
3 protects body fr disease-causing pathogens

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2
Q

3 functions of Immunity

A

1 recognize/remove abnormal self cells
2 removal of dead/damaged cells
3 protects body fr disease-causing pathogens

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3
Q

2 Primary Lymphoid Tissues

sites where immunity cells form + mature

A

1 Thymus Gland

2 Bone Marrow

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4
Q

Secondary Lymphoid Tissues

A

1 Encapsulated Lymphoid Tissues (spleen + lymph nodes)
2 Unencapsulated Diffuse Lymphoid Tissues [skin, MALT (mucosa-associated lymphoid tissues), GALT (gut-associated lymphoid tissue)]

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5
Q

Leukocytes

A
  • primary immune cells
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6
Q

Phagocytic Leukocytes

A 
1 Neutrophils (primary phagocyte)
2 Macrophages (primary phagocyte)
3 Dendritic Cells (link innate + adaptive immunity)
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7
Q

Antigen-Presenting Cells (APCs)

A

phagocytic cells that return digested antigen peptide to APC membrane combined w MHC class II

  • macrophage + dendritic cell
  • dendrites w antigen migrates to lymphoid tissues to present the antigen to lymphocytes
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8
Q

Antigen-Presenting Cells

A

1 macrophages

2 dendritic cells

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9
Q

Basophils

Mast Cells in tissues

A

-release chem that contribute to inflammation + innate immune response

Mast Cells are concentrated in connective tissues of lungs, skin, GI tract)

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10
Q

Eosinophil

A
  • found in GI tract, lungs, urinary/genital epithelia, + connective tissue of skin
  • attach to large antibody-coated parasites and release their granules into them
  • allergic rxn - inflammation + tissue damage
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11
Q

Neutrophil

A
  • phagocytic cells that ingest + kill 5-20 bacterias, release cytokines, chem mediators in inflammatory response
  • short lifespan of 1-2 days
  • most abundant (50-70% of WBC)
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12
Q

Monocytes

A
  • monocytes are precursor to macrophages
  • spend only 8 hrs in circulation to move fr bone marrow to target tissue
  • in tissue, they enlarge + differentiate into Macrophage
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13
Q

Macrophage

A
  • phagocytic; primary scavengers
  • some patrol, some fixed
  • larger/more effective than neutrophil (ingest up to 100 bacteria)
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14
Q

Lymphocyte

A
  • 20-30% of WBC=5%of all lymphocytes
  • 95% are found in lymphoid tissues
  • secretes CYTOKINES that targets immune + non-immune cells, + sometimes pathogens
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15
Q

2 Primary Lymphoid Tissues

sites where immunity cells form + mature

A

1 Thymus Gland

2 Bone Marrow

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16
Q

Secondary Lymphoid Tissues

A

1 Encapsulated Lymphoid Tissues (spleen + lymph nodes)
2 Unencapsulated Diffuse Lymphoid Tissues [skin, MALT (mucosa-associated lymphoid tissues), GALT (gut-associated lymphoid tissue)]

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17
Q

Leukocytes

A
  • primary immune cells
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18
Q

6 Types of Leukocytes

never let monkeys eat bananas, Dummy

A 
1 Neutrophil
2 Lymphocytes
3 Monocytes (turns into Macrophage)
4 Eosinophils
5 Basophils
6 Dendritic Cells
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19
Q

Phagocytic Leukocytes

A

1 Neutrophils
2 Macrophages
3 Dendritic Cells

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20
Q

Antigen-Presenting Cells

A

1 macrophages

2 dendritic cells

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21
Q

Molecules of Innate Immune Response

A

Chemotaxins (signal moles that attract leukocytes to help)
Opsonins (moles that coat foreign particles to make them visible to phagocytes)
Pyrogens (raise body temp by altering hypothalamic setpoint)
Acute-Phase Proteins (increased concentration of various plasma proteins during the acute/early phase)

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22
Q

Eosinophil

A
  • found in GI tract, lungs, urinary/genital epithelia, + connective tissue of skin
  • attach to large antibody-coated parasites and release their granules into them
  • allergic rxn - inflammation + tissue damage
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23
Q

Neutrophil

A
  • phagocytic cells that ingest + kill 5-20 bacterias, release cytokines, chem mediators in inflammatory response
  • short lifespan of 1-2 days
  • most abundant (50-70% of WBC)
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24
Q

Monocytes

A
  • monocytes are precursor to macrophages
  • spend only 8 hrs in circulation to move fr bone marrow to target tissue
  • in tissue, they enlarge + differentiate into Macrophage
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25
Q

Macrophage

A
  • phagocytic; primary scavengers
  • some patrol, some fixed
  • larger/more effective than neutrophil (ingest up to 100 bacteria)
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26
Q

Molecules of Adaptive Immune Response

A

1 Major Histocompatibility Complex (MHC)
2 Antibodies
3 T-cell Receptors

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27
Q

Major Histocompatibility Complex (MHC)

A
  • family of membrane protein complexes encoded by a specific set of genes
  • proteins combine w peptide fragments of antigens that have been digested w/in the cell; MHC antigen-complex then binds to the surface of the cell so that the antigen is visible. MHC antigen-complex binds w/ T cell immune receptor
  • 2 classes
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28
Q

T + B lymphocytes

Maturation

A

Both are from the bone marrow. T goes to the thymus to mature.
B stays in the bone marrow; can mature to Plasma Cells

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29
Q

MHC class II molecules

A

found promarily on antigen-presenting cells

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30
Q

Antonym for Antibodies

A

Immunoglobulins

globular proteins that participate in adaptive immune responses

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31
Q

Clone

A

group of lymphocytes that bind to that particular antigen.

Each B + T lymphocytes binds only to 1 particular antigen. If a pathogen appears, the clone who’s cell receptor match the pathogen quickly reproduces to provide the additional cells

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32
Q

Self-Tolerance

A

the lack of immune response by lymphocytes to the cells of the body so that the individual is not harmed

prevents autoimmune response

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33
Q

Hygiene Hypothesis

A

challenging the immune system early in life streghtens it

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34
Q

Acute-Phase Proteins

A
  • increased concentrations of various plasma proteins durint the acute phase (early phase)
  • normaly declines to normal as immune phases proceeds
  • acts as opsonins (coats particles for phagocytes to see), enzyme inhibitors (to prevent tissue damage), and C-reactive proteins (CRP)
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35
Q

C-reactive Proteins (CRP)

A

acute-phase protein

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36
Q

Histamine

A
  • found in granules of Mast Cells/Basophils
  • initiates inflammatory response
  • brings more leukocytes to injury site by dilating blood vessels to the area + opening pores on capillaries (more proteins leak into interstitial space, water follows, results w swelling)
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37
Q

Membrane Attack Complex

A

group of lipi-solulable proteins
-inserts themselves into cell membranes of pathogens/virus-infected cells; forms giant pores, allows water + ions to flow in; cell/pathogen swell, and lyse

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38
Q

Molecules of Adaptive Immune Response

A

1 Major Histocompatibility Complex (MHC)
2 Antibodies
3 T-cell Receptors

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39
Q

IgE

A
  • targets parasites + associated w allergic rxn

- mast cells binds w IgE + antigen, initiates degranulation + release chem mediators such as histamine

40
Q

IgM

A
  • associated w early immune response

- react to antigens found on red blood cells

41
Q

IgD

A

-appear as receptors on surface of B lymphocytes + help activate B ymphocytes

42
Q

T cell Receptors

A
  • not antibodies

- binds only to MHC antigen complex

43
Q

Virus

A

Structure: not cells, nucleic acid core in protein capsid; some have external envelopes
Conditions: needs host to reproduce
Genes: DNA or RNA
Drugs:cant be killed w antibiotics. can be suppressed w antiviral

44
Q

Fc Region

Antibody Anatomy

A
  • stem of Y shaped Antibody

- determines the class to which the antibody belongs

45
Q

Hinge Region

Antibody Anatomy

A

Between the arms and stem

allows for flexibility

46
Q

Fab Region

Antibody Anatomy

A
  • each arm of the Y shaped antibody

- contains 1 light chain + 1 heavy chain + 1 antigen binding site

47
Q

5 Classes of Antibodies/Immunoglobulins (Ig)

A 
IgG
IgA
IgE
IgM
IgD
48
Q

IgG

A
  • 75% of plasma antibody in adults

- in babies, some msternal IgG moves across the placenta to provide a few months of immunity

49
Q

IgA

A
  • found in external secretions like saliva, tears, intestinal + bronchial mucus, + breast milk
  • bind to pathogen + flag for phagocytosis if reaches the internal environment
50
Q

Bacteria

A

Structure: cells w cell wall. no organelles
Conditions: can survive + reproduce outside of host
Genes: singular circular DNA chromosome
Drugs: can be killed/suppresed w antibiotics

51
Q

Virus

A

Structure: not cells, nucleic acid core in protein capsid; some have external envelopes
Conditions: needs host to reproduce
Genes: DNA or RNA
Drugs:cant be killed w antibiotics. can be suppressed w antiviral

52
Q

BARRIERS: first line of defense

A

epithelium, glandular secretioin (mucus, antibodies, enzymes), stomach acidity, mechanical removal (mucociliary escalator, tears, cough/sneeze, GI motility)

53
Q

Interferons

A

interfered w viral replication by promoting synthesis of antiviral proteins

54
Q

Adaptive Immune Response

A

-antigen-specific response in which body recognized the particular foreign substance + selectively reacts to it

2 types: PASSIVE + ACTIVE IMMUNITY

55
Q

Phagocytes

A

-engulf + ingest their targets by phagocytosis
-receptor mediated event
-

56
Q

Pathogen-Associated Molecular Pattern (PAMPs)

A

classes of molecules that are uniqure to microorganisms
-binds to leukocyte’s pattern-recognition-receptors + activate responses that attempt to kill or ingest the invader (phagocytosis)

57
Q

Effector Cells

A

carry out immediate response, then die w/in a few days

-b cells turn into effector cells which either turn into memory to plasma cells

58
Q

Cytokines + Inflammatory Response

3 Roles

A

1 attract immune cells + chem mediators on site
2 produce physical barrier to retard the spread of infection
3 promote tissue repair once infection is under control

59
Q

PRIMARY IMMUNE RESPONSE

A
  • triggered by initial exposure of a naive lymphocyte clone to its antigen
  • activated lymphocyte undergoes clonal expansion creating new EFFECTOR CELLS (some differentiate into plasma cells)
60
Q

Cytokine

A

-attract additional immune cells, increase capillary permeability (leakage of ions, water follows, results in swelling), cause fever
NK secretes many cytokines like INTERFERONS

61
Q

Interferons

A

interfered w viral replication by promoting synthesis of antiviral proteins

62
Q

Adaptive Immune Response

A

-antigen-specific response in which body recognized the particular foreign substance + selectively reacts to it

63
Q

Naive Lymphocytes

A
  • a few cells that represents each clone of lymphocytes at birth
  • small # of cells in each naive clone arent enough to fight off foreign invaders
  • first exposure to antigen activates appropriate clone to reproduce
64
Q

Antibody Functions

A 
1 antigen clumping
2 inactivation of bacterial toxins
3 act as opsonins to tag antigens for phagocytosis
4 trigger degranulation
5 activate complement
6 activate B lymphocytes
65
Q

Effector Cells

A

carry out immediate response, then die w/in a few days

66
Q

Memory Cells

A
  • second/subsequent exposures to the antigen activates MEMORY CELLS to cause rapid clonal expansion;
  • quicker/stronger secondary response to antigen than first exposure
  • long lived, continues to reproduce itself
67
Q

Lyphocyte Secretions

A

B CELL > PLASMA CELL secretes ANTIBODIES
T CELL secretes
NK KILLER

68
Q

Plasma Cells

A

B cells > Plasma Cells; they lose their B cell receptors on their membranes

-begins to secrete antibodies to create HUMORAL IMMUNITY

69
Q

T Lymphocyte subtypes

A

Cytotoxic T Cells
Helper T Cells
Regulatory T Cells

70
Q

B Cells post immune response

A
  • antibody production becomes slower + lower
  • most short-lived plasma cells die off
  • a few long-lives plasma cells remain in bone marrow secreting low levels of antibodies for continued immunity
  • some B cells become MEMORY B CELLS that stay alive waiting for next reexposure
71
Q

SECONDARY IMMUNE RESPONSE

A

quicker/larger becomes of memroy cells that remained fr first exposure

72
Q

Antibody Functions

A 
1 antigen clumping
2 inactivation of bacterial toxins
3 act as opsonins to tag antigens for phagocytosis
4 trigger degranulation
5 activate complement
6 activate B lymphocytes
73
Q

Antibody-Dependant Cell-Mediated Cytotoxicity

A

when NK cells degranulate + destroy anibody-tagged pathogens

-combo of antigen, antibody, +cell receptords trigger degranulation

74
Q

PASSIVE IMMUNITY

A
  • type of adaptive immunity
  • when we acquire antibodies made by another organism
    ex) transfer of antibodies fr mother to fetus, gamma globulin (antibodies extracted fr donated human plasma)
75
Q

ACTIVE IMMUNITY

A
  • type of adaptive immunity
  • occurs when body is exposed to a pathogen + body produces its own antibodies
  • can occur naturally or artificially (like w a vaccine of dead/disabled pathogens)
76
Q

VACCINE

A

altered pathogen that no longer harms the host, can be recognized as foreign by immune cells
-triggers a creation of memory cells specific to that pathogen so that if the person is exposed, then memory cells can produce stronger + faster secondary immune response.

77
Q

Cytotoxic T Cells

A

responsible for cell-mediated immunity that defends the body against inracellular pathogens

-once pathogen gets inside a host cell, antibodies are not longer effective (can only bind to exposed antigens)

78
Q

Cytotoxic T Cells induce apoptosis in 2 ways

A
  1. release cytotoxic pore-forming molecules called PERFORIN along w GANZYMES
  2. activate Fas (death receptor protein) on target cell membrane
79
Q

GRANZYMES

A
  • enzymes related to the digestive enzymes trypsin and chymotrypsin
  • when granzyes enter perforin channels, they activate apoptosis
80
Q

Helper T Cells

A
  • binds to immune cells that display foreign antigen in MHC II complexes to activate Helper T Cells to secrete CYTOKINES
  • does not directly attack pathogens + infected cells
81
Q

Regulatory T Cells

A
  • binds to MHC II complexes to suppress immine cell functions
  • helps prevent excessive immune resonse

-does not directly attack pathogens + infected cells

82
Q

Complement System

A

componenets of the bacterial cell wall are antigens that activate the complement system:

  • acts as opsonins
  • cause degranulation of mast cells w histamine release
  • acts as chemotaxins
  • form membrane attack complex molecules that insert themselves into the wall of unencapsulated bacteria (creates influx of ions, water follows, cell lyses)
83
Q

Viral Infection INTRACELLULAR DEFENSE

A

T lymphocytes + NK cells becomes the main defense against intracellular viruses

84
Q

Allergy

A

inflammatory immune response to nonpathogenic antigen

  • allergic response can range fr mild tissue damage to fatal rxn
  • strong genetic component - If parents have a specific allergy, their children are likely to have the same
85
Q

Allergen

A

an antigen that is typically not harmful to the body

86
Q

Sensitivity/Hypersensitivity

A

immune response in allergies

87
Q

Immediate Hypersensitivity Rxn

A

mediated by antibodies and occur w/in minutes of exposure to allergens

88
Q

Delayed Hypersensitivity Rxn

A

mediated by Helper T Cells + Macrophages

  • may take days to develop
  • includes contact allergies to copper, and other base metals
89
Q

Anaphylaxis

A

mose severe IgE-mediated allergic rxn
-increase in mast degranulation >increase in histamine levels>vasodilation, circulatory collapse, and sever bronchoconstriction

+must be treated w EPINEPHRINE in 20 mins

90
Q

Human Leukocyte Antigens (HLA)

aka MHC proteins

A
  • tissue graft/transpplant is likely to be succesful if the donor + recipient share HLA antigens
  • incompatible matches trigger antibody production, activates cytotoxic + helper T cells
91
Q

ABO Blood groups

A

O - no A/B antigens; has anti A anti B antibodies in plasma
A - A antigens; anti B antibodies in plasma
B - B antigens; anti A antibodies in plasma
AB - AB antigens; no antibodies in plasma

92
Q

Rhesus D Blood Groups

A

Rh+ has D antigen
Rh- no D antigen

-someone who is Rh- that is exposed to foregin D antigen, will makke D antibodies

93
Q

Hemolytic Disease of Newborn aka Ertyhroblastosis Fetalis

A

blood type incompatibilies w mother + fetus due to blood transfer

94
Q

Immune Sytem Pathologies

A

1 Incorrect Response - autoimmune disease
2 Overreactive Response - allergies/ hypersensitivity
3 Lack of Response - immunodeficiency disease when some component of immune system fails

95
Q

Autoimmune Disease

A

when the body makes antibodies against its own components though T-cell-activated Blymphocytes

-results w body attacking itself

ex) diabetes mellitus - body makes islet cell antibodies that destroys pancreatic beta cells.
hyperthyroidism of Grave’s disease - leads to oversecretion of thyroid

96
Q

Immune Surveilance

A

abnorml cells are detected by the immune system and destroyed before they spread

97
Q

Neuroimmunomodulations aka

Psychoimmunology

A

study of brain - immune interactions

PHYS 261 (4 decks)

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