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► Med - Anatomy & Physiology > Immune System > Flashcards

Immune System Flashcards

1
Q

Resistance to disease

A

Immunity

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2
Q

Two intrinsic systems of immunity

A
  1. Innate (nonspecific) defense system

2. Adaptive (specific) defense system

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3
Q

Two lines of defense in the innate system

A

–First - external body membranes (skin and mucosae)

–Second - antimicrobial proteins, phagocytes, and other cells
•Inhibit spread of invaders
•Inflammation most important mechanism

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4
Q

Line of defense in the adaptive system

A

–Third line of defense attacks particular foreign substances

•Takes longer to react than innate system

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5
Q

Ward off invading pathogens

A

Surface Barriers

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6
Q

Types of surface barriers

A

Skin, mucous membranes, and their secretions

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7
Q

Three functions of surface barriers

A
  1. Physical barrier to most microorganisms
  2. Keratin resistant to weak acids and bases, bacterial enzymes, and toxins
  3. Mucosae provide similar mechanical barriers
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8
Q

Four protective chemicals of surface barriers that inhibit or destroy microorganisms

A
  1. Acidity of skin and secretions – acid mantle – inhibits growth
  2. Enzymes - lysozyme of saliva, respiratory mucus, and lacrimal fluid – kill many microorganisms
  3. Defensins – antimicrobial peptides – inhibit growth
  4. Other chemicals - lipids in sebum, dermcidin in sweat – antimicrobial toxin
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9
Q

Respiratory system modifications

A

–Mucus-coated hairs in nose

–Cilia of upper respiratory tract sweep dust- and bacteria-laden mucus toward mouth

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10
Q

When surface barriers are breached by nicks or cuts

A

Second line of defense must protect deeper tissues

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11
Q

Five necessary internal defenses if microorganisms invade deeper tissues

A
  1. Phagocytes
  2. Natural killer (NK) cells
  3. Antimicrobial proteins (interferons and complement proteins)
  4. Fever
  5. Inflammatory response (macrophages, mast cells, WBCs, and inflammatory chemicals)
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12
Q

Phagocytes

A

Neutrophils

Macrophages

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13
Q

Become phagocytic on exposure to infectious material. Most abundant but die fighting.

A

Neutrophils

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14
Q

Develop from monocytes – chief phagocytic cells – robust cells

A

Macrophages

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15
Q

Two types of macrophages

A
  1. Free

2. Fixed

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16
Q

Wander through tissue spaces, e.g., alveolar macrophages

A

Free Macrophages

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17
Q

Permanent residents of some organs; e.g., Kupffer cells (liver) and microglia (brain)

A

Fixed Macrophages

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18
Q

Some microorganisms evade adherence with …

A

Capsule

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19
Q

Opsonization

A

Targeting (marking) a pathogen for deletion

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20
Q

Mechanism of Phagocytosis

A
  1. Phagocyte must adhere to particle
  2. Pathogens killed by acidifying and digesting with lysosomal enzymes
  3. Helper T cells cause release of enzymes that produce the respiratory burst, which kill pathogens resistant to lysosomal enzymes by
    –Releasing cell-killing free radicals
    –Producing oxidizing chemicals (e.g., H2O2)
    –Increasing pH and osmolarity of phagolysosome
  4. Defensins (in neutrophils) pierce membrane
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21
Q

Natural Killer (NK) Cells

A

•Nonphagocytic large granular lymphocytes

•Attack cells that lack “self” cell-surface receptors
–Induce apoptosis in cancer cells and virus-infected cells

•Secrete potent chemicals that enhance inflammatory response

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22
Q

Inflammatory Response

A
  • Triggered whenever body tissues injured
  • Prevents spread of damaging agents
  • Disposes of cell debris and pathogens
  • Alerts adaptive immune system•Sets the stage for repair
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23
Q

Cardinal signs of acute inflammation

A
  1. Redness
  2. Heat
  3. Swelling
  4. Pain

(Sometimes 5. Impairment of function)

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24
Q

Edema

A

Increased capillary permeability –> exudate to tissues –> local swelling –> pain –> moves foreign material to lymphatics –> delivers clotting proteins

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25
Q

Produced by the liver in response to inflammatory molecules

A

C-reactive Protein (CRP)

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26
Q

CRP is a clinical marker used to assess:

A
  1. The presence of an acute infection

2. An inflammatory condition and its response to treatment

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27
Q

Steps for phagocyte mobilization

A
  1. Leukocytosis
  2. Margination
  3. Diapedesis
  4. Chemotaxis
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28
Q

Release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells

A

Leukocytosis

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29
Q

Neutrophils cling to walls of capillaries in inflamed area in response to CAMs (cell adhesion molecules)

A

Margination

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30
Q

Neutrophils squeeze through capillary walls and begin phagocytosis

A

Diapedesis

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31
Q

Inflammatory chemicals (chemotactic agents) promote positive chemotaxis of neutrophils

A

Chemotaxis

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32
Q

Functions of interferons and complement proteins

A
  1. Attack microorganisms directly

2. Hinder microorganisms’ ability to reproduce

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33
Q

Family of immune modulating proteins

A

Interferons (IFNs)

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34
Q

Viral-infected cells secrete …

A

IFNs to “warn” neighboring cells

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35
Q

Immune Interferon

A

IFN Gamma

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36
Q

Three functions of IFN Gamma

A
  1. Secreted by lymphocytes
  2. Widespread immune mobilizing effects
  3. Activates macrophages
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37
Q

Function of Alpha and Beta IFNs

A

Activate NK cells and macrophages, indirectly fight cancer

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38
Q

Artificial IFNs used to treat …

A

Hepatitis C, genital warts, multiple sclerosis, hairy cell leukemia

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39
Q

Complement System

A
  • ~20 blood proteins that circulate in inactive form
  • Our cells contain complement activation inhibitors
  • Enhances both innate and adaptive defenses
  • Unleashes inflammatory chemicals that amplify all aspects of inflammatory response
  • Promotes phagocytosis
  • Kills bacteria and certain other cell types by cell lysis
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40
Q

Fever

A
  • Abnormally high body temperature
  • Systemic response to invading microorganisms
  • Leukocytes and macrophages exposed to foreign substances secrete pyrogens
  • Pyrogens act on body’s thermostat in hypothalamus, raising body temperature
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41
Q

Why high fevers are dangerous

A

Can denature enzymes

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42
Q

Benefits of moderate fever

A
  1. Causes liver and spleen to sequester iron and zinc (needed by microorganisms)
  2. Increases metabolic rate –> faster repair
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43
Q

Recognizes and targets specific antigens

A

Specific Defense

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44
Q

Not restricted to initial site

A

Systemic Defense

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45
Q

Stronger attacks to “known” antigens

A

Memory Defense

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46
Q

Two separate overlapping arms of defense

A
  1. Humoral (antibody-mediated) immunity (B-cell)

2. Cellular (cell-mediated) immunity (T-Cell)

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47
Q

Antigens

A
  • Substances that can mobilize adaptive defenses and provoke an immune response
  • Targets of all adaptive immune responses
  • Antigen = “antibody generator”
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48
Q

Two important properties of complete antigen function

A

–Immunogenicity

–Reactivity

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49
Q

Ability to stimulate proliferation of specific lymphocytes

A

Immunogenicity

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50
Q

Ability to react with activated lymphocytes and antibodies released by immunogenic reactions

A

Reactivity

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51
Q

Haptens

A
  • Small molecules not immunogenic by themselves (Incomplete Antigens)
  • May be immunogenic if attached to body proteins and combination is marked foreign
  • Cause immune system to mount harmful attack (hypersensitivity reaction)
  • Examples: poison ivy, animal dander, detergents, and cosmetics
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52
Q

Only certain parts of entire antigen are immunogenic

A

Antigenic Determinants

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53
Q

Antibodies and lymphocyte receptors bind to them as enzyme binds substrate

A

Antigenic Determinants

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54
Q

Protein molecules surface of cells not antigenic to self but antigenic to others in transfusions or grafts

A

Self-Antigens

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55
Q

One group of self-antigens

A

MHC Proteins (Major Histocompatibility Complex)

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56
Q

The two major classes of MHC proteins

A

–Class I MHC proteins – found on virtually all body cells except RBC’s

–Class II MHC proteins – found on certain cells in the immune response (Antigen Presenting cells)

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57
Q

Antigen presenting cells can have …

A

Class I and Class II MHC proteins

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58
Q

Three types of cells in the adaptive immune system

A
  1. B lymphocytes (B cells)—humoral immunity
  2. T lymphocytes (T cells)—cell-mediated immunity
  3. Antigen-presenting cells (APCs)
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59
Q

Antigen Presenting Cells

A
  • Do not respond to specific antigens
  • Play essential auxiliary roles in immunity
  • Engulf antigens
  • Present fragments of antigens to T cells for recognition
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60
Q

The ratio of T cells to B cells

A

3:1

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61
Q

B cells mature in the …

A

Bone Marrow

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62
Q

T cells mature in the …

A

Thymus

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63
Q

Three major types of Antigen Presenting Cells

A

–Dendritic cells in connective tissues and epidermis

–Macrophages in connective tissues and lymphoid organs

–B cells

64
Q

Dendritic Cells

A

–Phagocytize pathogens, enter lymphatics to present antigens to T cells in lymph node

–Most effective antigen presenter known

–Activate naïve T cells

65
Q

Macrophages

A

–Widespread in lymphoid organs and connective tissues

–Can activate naive T cells

–Present antigens to T cells to activate themselves into voracious phagocytes that secrete bactericidal chemicals

66
Q

B Cells

A

–Do not activate naive T cells

–Present antigens to helper T cell to assist own activation

67
Q

Five stages of lymphocyte delevopment

A
  1. Origin – all originate in red bone marrow
  2. Maturation
  3. Seeding secondary lymphoid organs and circulation
  4. Antigen encounter and activation
  5. Proliferation and differentiation
68
Q

Lymphocyte can recognize one specific antigen by binding to it

•B or T cells display unique receptor on surface when achieve maturity – bind only one antigen

A

Immunocompetence

69
Q

Lymphocytes unresponsive to own antigens

A

Self-Tolerance

70
Q

Pressure tests under which T Cells mature in the Thymus

A

Positive selection

Negative selection

71
Q

Positive Selection

A

Selects T cells capable of recognizing self-MHC proteins (MHC restriction); failures destroyed by apoptosis

72
Q

Negative Selection

A
  • Prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC
  • Ensures self-tolerance
73
Q

Percent of T-cells that survive the selection process

A

2%

74
Q

Self-reactive B Cells

A
  1. Are eliminated by apoptosis (clonal deletion) or
  2. Undergo receptor editing – rearrangement of their receptors
  3. Are inactivated (anergy) if they escape from the bone marrow
75
Q

Immunocompetent B and T cells not yet exposed to antigen

A

Naive

76
Q

Determine which foreign substances immune system will recognize

A

Genes

77
Q

Make up to a billion different types of antigen receptors–coded for by ~25,000 genes

A

Lymphocytes

78
Q

Clonal Selection

A

–Naive lymphocyte’s first encounter with antigen (antigen challenge) –> selected for further development

–If correct signals present, lymphocyte will complete its differentiation

79
Q

Steps of lymphocyte proliferation

A
  • Activated lymphocyte proliferates –> exact clones
  • Most clones –> plasma cells (effector cells) that fight infections
  • Some become memory cells–Able to respond to same antigen more quickly second time
80
Q

Most clone cells become …

A

Plasma cells

81
Q

Rate at which clone cells secrete specific antibodies

A

2000 molecules per second for four to five days, then die

82
Q

Clone cells that do not become plasma cells become

A

Memory cells

83
Q

Memory Cells

A

–Provide immunological memory

–Mount an immediate response to future exposures to same antigen

84
Q

Primary Immune Response

A

–Cell proliferation and differentiation upon first antigen exposure

–Lag period: three to six days

–Peak levels of plasma antibody are reached in 10 days

–Antibody levels then decline

85
Q

Secondary Immune Response

A

–Re-exposure to same antigen gives faster, more prolonged, more effective response

  1. Sensitized memory cells respond within hours
  2. Antibody levels peak in two to three days at much higher levels
  3. Antibodies bind with greater affinity
  4. Antibody level can remain high for weeks to months
86
Q

When B cells encounter antigens and produce specific antibodies against them

A

Active Humoral Immunity

87
Q

Two types of active humoral immunity

A

–Naturally acquired—response to bacterial or viral infection

–Artificially acquired—response to vaccine of dead or attenuated(living, but extremely weakened) pathogens

88
Q

Vaccines

A

–Most contain dead or attenuated pathogens

–Spare us symptoms of primary response

–Provide antigenic determinants that are immunogenic and reactive

–Can cause illness trying to vaccinate against; can cause allergic responses

89
Q

Passive Humoral Immunity

A
  • Readymade antibodies introduced into body
  • B cells are not challenged by antigens
  • Immunological memory does not occur
  • Protection ends when antibodies degrade
90
Q

Two types of passive humoral immunity

A

1.Naturally acquired—antibodies delivered to fetus via placenta(IgG) or to infant through milk(IgA)

2.Artificially acquired—injection of serum, such as gamma globulin
•Protection immediate but ends when antibodies naturally degrade in body

91
Q

Proteins also know as Immunoglobulins—gamma globulin portion of blood

A

Antibodies

92
Q

Capable of binding specifically with antigen detected by B cells

A

Antibodies

93
Q

Five classes of antibodies

A

IgM

IgA

IgD

IgG

IgE

94
Q

IgM

A

–First antibody released

–Potent agglutinating agent

–Readily fixes and activates complement

–Has the highest avidity (affinity)

–Found on the surface of B cells as receptors

95
Q

IgA

A

–In mucus and other secretions including saliva, tears, and colostrum (found in breast milk)

–Helps prevent entry of pathogens

96
Q

IgD

A

–Attached to surface of B cells

–Functions as B cell receptor

97
Q

IgG

A

–Monomer; 75–85% of antibodies in plasma

–From secondary and late primary responses

–Crosses placental barrier

98
Q

IgE

A

–Monomer active in some allergies (Type I Hypersensitivity) and parasitic infections

99
Q

B cells can switch antibody classes but retain …

A

Antigen specificity

100
Q

Almost all secondary responses are …

A

IgG

101
Q

Inactivate and tag antigens; they do not destroy them

A

Antibodies

102
Q

Four defense mechanisms used by antibodies

A

–Neutralization and agglutination (the two most important)

–Precipitation and complement fixation

103
Q

Neutralization

A
  • Simplest defensive mechanism
  • Antibodies block specific sites on viruses or bacterial exotoxins
  • Prevent these antigens from binding to receptors on tissue cells
  • Antigen-antibody complexes undergo phagocytosis
104
Q

Agglutination

A
  • Antibodies bind same determinant on more than one cell-bound antigen
  • Cross-linked antigen-antibody complexes agglutinate
105
Q

Precipitation

A
  • Soluble molecules are cross-linked

* Complexes precipitate and are subject to phagocytosis

106
Q

Complement Fixation

A

•Main antibody defense against cellular antigens (bacteria, mismatched RBCs)

•Several antibodies bind close together on a cellular antigen –> complement-binding sites on stem regions align
–Triggers complement fixation into cell’s surface
– Cell lysis

107
Q

Activated complement functions

A

–Amplifies inflammatory response

–Promotes phagocytosis via opsonization

–Positive feedback cycle that enlists more and more defensive elements

108
Q

Summary of antibody actions

A
  • Antigen-antibody complexes do not destroy antigens; prepare them for destruction by innate defenses
  • Antibodies do not invade solid tissue unless lesion present
  • Can act intracellularly if attached to virus before it enters cell –Activate mechanisms that destroy virus
109
Q

Cellular immune response

A
  • T cells provide defense against intracellular antigens

* Some T cells directly kill cells; others release chemicals that regulate immune response

110
Q

Two populations of T cells based on which glycoprotein surface receptors displayed

A

CD4 and CD8

111
Q

CD4 Cells

A

Usually become helper T cells (TH); activate B cells, other T cells, macrophages, and direct adaptive immune response

•Some become regulatory T cells (suppressor T) – which moderate immune response

–Can also become memory T cells

112
Q

CD8 Cells

A

Become cytotoxic T cells (TC)

  • Destroy cells harboring foreign antigens
  • Also become memory T cells
113
Q

Activated T Cells

A

Helper, cytotoxic, and regulatory T cells

114
Q

Two types of MHC proteins important to T cell activation

A

–Class I MHC proteins – displayed by all cells except RBCs •Recognized by CD 8 (cytotoxic T) cells

–Class II MHC proteins – displayed by APCs (dendritic cells, macrophages, and B cells) •Recognized by CD4 (helper T)cells

115
Q

Primary T cell response peaks within …

A

One week

116
Q

T cell apoptosis occurs between …

A

Day 7 and 30

117
Q

Benefit of apoptosis

A

Activated T cells are a hazard – produce large amount of inflammatory cytokines –> hyperplasia, cancer

118
Q

Memory T cells

A

Remain and mediate secondary responses

119
Q

Cytokines

A
  • Chemical messengers of immune system–Mediate cell development, differentiation, and responses in immune system
  • Include interferons and interleukins
120
Q

Interleukin 1 (IL-1)

A

Released by macrophages, co-stimulates bound T cells to

–Release interleukin 2 (IL-2)
–Synthesize more IL-2 receptors

121
Q

Interleukin 2 (IL-2)

A

Key growth factor, acting on cells that release it and other T cells

–Encourages activated T cells to divide rapidly
–It is used therapeutically to enhance the body’s defenses against cancer (melanoma & kidney)

122
Q

Roles of Helper T cells

A

•Play central role in adaptive immune response
–Activate both humoral and cellular arms
•Stimulate B cells to divide more rapidly and begin antibody formation
•Without TH, there is no immune response

123
Q

Once Helper T Cells are primed by APC presentation of antigen, they …

A
  1. Help activate T and B cells
  2. Induce T and B cell proliferation
  3. Their cytokines recruit other immune cells
124
Q

B cells may be activated without TH cells by binding to

A

T cell–independent antigens

–Response weak and short-lived

125
Q

Most antigens require TH co-stimulation to activate B cells

A

T cell–dependent antigens

126
Q

Require TH cell to activate into destructive cytotoxic T cells

A

CD8 Cells

127
Q

Cause dendritic cells to express co-stimulatory molecules required for CD8 cell activation

A

TH Cells

128
Q

Required for activation of CD8 cells to become Tc cells.

A

Vitamin D

129
Q

Amplify responses of innate immune system

–Activate macrophages –> more potent killers

–Mobilize lymphocytes and macrophages and attract other types of WBCs

A

Helper T Cells

130
Q

Cytotoxic T Cells

A
  • Directly attack and kill other cells
  • Activated TC cells circulate in blood and lymph and lymphoid organs in search of body cells displaying antigen they recognize
131
Q

Four cytotoxic T cell targets

A
  1. Virus-infected cells
  2. Cells with intracellular bacteria or parasites
  3. Cancer cells
  4. Foreign cells (transfusions or transplants)
132
Q

Two methods of lethal hit by cytotoxic T cells

A

1.TC cell releases perforins and granzymes by exocytosis
•Perforins create pores through which granzymes enter target cell
•Granzymes stimulate apoptosis

2.TC cell binds specific membrane receptor on target cell, and stimulates apoptosis

133
Q

Though non-specific use the same key mechanisms as TC cells for killing their target cells

A

Natural Killer Cells

134
Q

Two ways regulatory T cells dampen immune response

A
  1. direct contact

2. inhibitory cytokines

135
Q

Regulatory T Cells

A

Important in preventing autoimmune reactions

–Suppress self-reactive lymphocytes in periphery (outside lymphoid organs)

136
Q

Four major types of grafts

A
  1. Autografts (self): from one body site to another in same person
  2. Isografts (same): between identical twins
  3. Allografts (other): between individuals who are not identical twins
  4. Xenografts (foreign): from another animal species
137
Q

Success of organ transplants depends on …

A

Similarity of tissues

138
Q

Ideal donor tissues

A

Autografts and Isografts

139
Q

Most common donor tissue

A

Allografts

•ABO, other blood antigens, MHC antigens matched as closely as possible

140
Q

Prevention of rejection after transplant surgery

A

–Patient treated with immunosuppressive therapy

  1. Corticosteroid drugs to suppress inflammation
  2. Antiproliferative drugs
  3. Immunosuppressant drugs
141
Q

Severe side effect of immunosuppressant drugs

A

Depress patient’s immune system so it cannot fight off foreign agent

142
Q

Condition that impairs function or production of immune cells or molecules such as complement or antibodies

A

Immunodeficiency (congenital or acquired)

143
Q

–Marked deficit in B and T cells

–Defective adenosine deaminase (ADA) enzyme •Metabolites lethal to T cells accumulate

–Fatal if untreated; treated with bone marrow transplants

A

Severe Combined Immunodeficiency (SCID) Syndrome - genetic defect

144
Q
  • Acquired immunodeficiency
  • Cancer of B cells
  • Leads to immunodeficiency by depressing lymph node cells
A

Hodgkin’s Disease

145
Q
  • Cripples immune system by interfering with activity of helper T cells
  • Opportunistic infections occur, including pneumocystis pneumonia and Kaposi’s sarcoma
  • Caused by human immunodeficiency virus (HIV), a retrovirus, transmitted via body fluids—blood, semen, and vaginal secretions
A

Acquired Immune Deficiency Syndrome (AIDS)

146
Q

–Destroys TH cells –> depresses cell-mediated immunity
• Multiplies in lymph nodes throughout asymptomatic period, ~10 years if untreated
•97% percent of persons will develop antibodies in the first 3 months following the time of their infection.

A

HIV

147
Q
  • Enters cell and uses reverse transcriptase to produce DNA from its viral RNA
  • The DNA copy (a provirus) directs host cell to make viral RNA and proteins, enabling virus to reproduce
  • Reverse transcriptase –> frequent errors (transcription errors); high mutation rate and resistance to drugs
A

HIV

148
Q

Four antiviral drug treatments for HIV

A
  1. Fusion inhibitors block HIV’s entry into cell
  2. Integrase inhibitors block viral RNA integration into host’s DNA
  3. Reverse transcriptase and protease inhibitors inhibit viral replication enzymes
  4. Antiretroviral vaginal gel reduces risk by 50%
149
Q

Autoimmune Diseases

A
  • Immune system loses ability to distinguish self from foreign
  • 5%of adults in North America (two-thirds women) have an autoimmune disease
  • Production of autoantibodies and sensitized TC cells that destroy body tissues
150
Q

Weakly self-reactive lymphocytes may be activated by

A

–Foreign antigens may resemble self-antigens
•Antibodies against foreign antigen may cross-react with self-antigen

–New self-antigens may appear, generated by

  1. Gene mutations
  2. Changes in self-antigens by hapten attachment or infectious damage
  3. Release of novel self-antigens by trauma to barrier
151
Q

Hypersensitivities

A
  • Immune responses to perceived (otherwise harmless) threat that causes tissue damage
  • Different types distinguished by
  1. Their time course
  2. Whether antibodies or T cells involved
  • Antibodies cause immediate and subacute hypersensitivities (Type I,II, and III)
  • T cells cause delayed hypersensitivity (Type IV)
152
Q

Acute (type I) hypersensitivities (allergies) (Immediate)

A
  • Begin in seconds after contact with allergen
  • Initial contact is asymptomatic but sensitizes person
  • Reaction may be local (skin, resp, GI) or systemic (anaphylaxis)
153
Q

Cytotoxic (type II) reactions (subacute)

A
  • Caused by IgM and IgG transferred via blood plasma or serum
  • Slow onset (1–3 hours) and long duration (10–15 hours)
  • Antibodies bind to antigens on specific body cells, stimulate phagocytosis and complement-mediated lysis of cellular antigens
154
Q

Immune complex (type III) hypersensitivity (subacute)

A

–Insoluble antigen-antibody complexes form
–Complexes cannot be cleared from particular area of body
–Intense inflammation, local cell lysis, and cell killing by neutrophils

155
Q

Delayed Hypersensitivities (Type IV)

A
  • Slow onset (one to three days)
  • Cytokine-activated macrophages and cytotoxic T cells cause damage
  • Agents act as haptens
  • TB skin test depends on this reaction
156
Q

Influences on immune system function

A

–Nervous system – depression, emotional stress, and grief impair immune response

–Diet – vitamin D required for activation of CD8 cells –> TC cells

► Med - Anatomy & Physiology (130 decks)

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