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PHGY 209 > IMMUNOLOGY > Flashcards

IMMUNOLOGY Flashcards

1
Q

What occurs at the Primary Lymphoid Organs

A

Sites where stem cells divide and immune cells develop

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2
Q

What occurs at the Secondary Lymphoid Organs

A

Sites where most immune responses occur

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3
Q

Primary Lymphoid Organs

A
  • Bone Marrow (Yolk Sac and Fetal Liver in Embryo)

- Thymus

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4
Q

Secondary Lymphoid Organs

A
  • lymph nodes
  • spleen
  • lymphoid nodules
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5
Q

Bone Marrow site where

A

B-cells mature

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6
Q

Thymus site where

A

T cells mature

Atrophies after maturity

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7
Q

The thymus contains what types of cells

A

Contains T cells, scattered dendritic cells, epithelial cells, and macrophages

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8
Q

Produced in the bone marrow

A

Blood cells are produced here: B-cells and Immature T-cells

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9
Q

Yolk Sac and Fetal Liver produces

A

Blood cells are produced here in the embryo

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10
Q

Lymph nodes

A 
Secondary Lymphoid Organ:
Scattered throughout the body
Filter microbes
Macrophages in nodes phagocytize microbes
that pass through in the lymph fluid
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11
Q

Spleen

A

Secondary Lymphoid Organ:
Largest lymphoid organ
Removes microbes and dead or old erythrocytes

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12
Q

Lymphoid Nodules

A

Secondary Lymphoid Organ:
Tonsils
Peyer’s Patches and MALT (Mucosal-Associated Lymphoid Tissues) Appendix

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13
Q

Immune Cells Travel in the ____ and _______

A

Immune Cells Travel in the Blood and Lymphatic Vessels

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14
Q

Immune Cells are

A

White Blood Cells/Leukocytes

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15
Q

Produced from lymphoid stem cells

A

Lymphocyte

  • T cells
  • B cells
  • NK cells
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16
Q

Produced from myeloid stem cells

A 
Erythrocyte
Neutrophil
Monocyte
Eosinophil
Basophil
Megakaryocyte (platelets(
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17
Q

Megakaryocyte produce

A

platelets

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18
Q

myeloid cells

A

Neutrophil
Monocyte
Eosinophil
Basophil

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19
Q

Macrophages and dendritic cells are

A

monocytes

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20
Q

Eosinophils

A

Destroy parasites

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21
Q

Basophils

A

Release a variety of chemicals Histamine, leukotrienes, prostaglandins

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22
Q

Mast Cells

A

Release chemicals, histamine

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23
Q

Neutrophils

A

Phagocytes

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24
Q

Monocytes

A

Macrophages and Dendritic Cells Phagocytes

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25
Q

Lymphocytes

A

B lymphocytes

T lymphocytes

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26
Q

T lymphocytes

A

TH and TC

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27
Q

Antigen

A
  1. Immunogen – material that induces an immune response 2. Hapten (+ Carrier = Immunogen)
  2. Allergen
  3. Tolerogen
  4. Ligand
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28
Q

Non-specific/Innate Immunity

A

Ability of the body to defend against microbes and other foreign substances - without recognition of the invading pathogen.

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29
Q

First Line of Defense

A

Physical Barriers

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30
Q

Second Line of Defense

A

Cellular Factors

Humoral Factors

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31
Q

Physical Barriers

A 
Skin
Mucus
Hair
Cilia
Sebum 
Lysozyme 
Gastric 
Juice
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32
Q

Innate Immunity

A

No memory

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33
Q

Cellular Factors (2nd Line of Defense)

A
  • Phagocytic Cells
    neutrophils, macrophages, dendritic cells
  • Cells with inflammatory mediators basophils, mast cells, eosinophils
  • Natural Killer Cells
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34
Q

Humoral Factors (2nd Line of Defense)

A
  • Inflammation and Fever
  • Antimicrobial Substances
    Acute Phase Reactants: C-Reactive Protein, Complement, Interleukin and Cytokines
  • Interferon-alpha
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35
Q

Non-Specific Response to Tissue Damage

A

Inflammation

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36
Q

4 Distinct Signs and Symptoms of Inflammation

A

Redness
Heat
Pain
Swelling

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37
Q

3 Stages of Inflammation

A
  1. Vasodilation*
  2. Emigration of Phagocytes
  3. Tissue Repair
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38
Q

Vasodilation

A
  • Widening of blood vessels allows more blood flow to the site
  • Increased permeability of capillaries allows substances to go to the damaged site
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39
Q

Antimicrobial Substances

A

Discourage Microbial Growth or Spread of Pathogen

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40
Q

Interferons

A

Binds to receptor on cells and sends signal to to activate genes for antiviral protien

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41
Q

Type I interferon

A

Prevents viral replication

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42
Q

Complement

A

a group of plasma proteins

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43
Q

Complement Protein Function

A

A large family of plasma proteins with multiple functions. 30 different proteins participate in the cascades.
A central protein in the complement cascade is C3.

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44
Q

A central protein in the complement cascade is

A

C3

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45
Q

Function of Complement C3b

A

As an opsonin

Binds to phagocytes via the C3b receptor

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46
Q

Natural Killer Cells

A

a class of lymphocytes, similar to cytotoxic T cells, who target virus-infected cells and cancerous cells

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47
Q

T/F: Natural Killer Cells attack and kill these target cells without binding to them.

A

F: they attack and kill these target cells directly after binding to them.

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48
Q

Natural Killer Cells are/are not antigen-specific

A

are not

NK cells do not need to recognize a specific antigen.

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49
Q

The similarity between cytotoxic T cells and NK cells

A

Like cytotoxic T cells, they attack and kill these target cells directly after binding to them.

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50
Q

How do NK cells kill body cells?

A

Release chemicals that lead to death of infected or abnormal body cells*
Release Perforin and granzyme

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51
Q

The difference between cytotoxic T cells and NK cells

A

Unlike cytotoxic T cells, they are NOT antigen-specific. NK cells do not need to recognize a specific antigen.

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52
Q

Perforin

A

polymerize and form a channel in target cell membrane

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53
Q

What do NK cells recognize on the cells

A

*Cells not expressing MHC-I
Virally-infected
or cancerous cells down-regulate MHC-1

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54
Q

What cells express MHC-I on their surface?

A

every nucleated cell in the body

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55
Q

Granzymes

A

induce programmed cell death (apoptosis) in the target cell

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56
Q

Phagocytes

A

Non-specifically engulf microbial invaders

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57
Q

Types of Phagocytes

A

Fixed-Tissue Macrophages Neutrophils

Monocytes – Macrophages and Dendritic Cells

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58
Q

Phagocytosis steps

A

Steps: Adherence, Ingestion, Digestion, Killing

  • Microbe
  • Endocytosis
  • phagosome formation
  • Lysosome fusion with the phagosome
  • Phagolysosome
  • Release of end products into or out of the cell
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59
Q

How Does the Phagocyte Recognize Microbes?

A

Detect unique, conserved proteins that are essential to microbial
physiology (molecular signatures of infection)

• Pathogen-Associated Molecular Patterns(PAMPs)

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60
Q

PAMPS are recognized by

A

Immune system receptors called pattern recognition receptors (PRR), including Toll-Like Receptors

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61
Q

Toll-Like Receptors

A

A family of highly conserved transmembrane receptors Essential for microbial recognition via PAMPs
• Extracellular domain for recognition of pathogens
• Intracellular signalling domain

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62
Q

Emigration of Neutrophils (phagocytes)

A

Chemotaxis
Margination –
Diapedesis –

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63
Q

Chemotaxis

A

Chemically stimulated movement of phagocytes

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64
Q

Chemoattractants

A

Chemicals that attract phagocytes

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65
Q

Margination

A

Migration of phagocyte towards the tissue injury

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66
Q

Diapedesis

A

Phagocytes move across the capillary wall

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67
Q

Specific Role of Neutrophils in Inflammation

A

Neutrophils Die in the Process of Killing Bacteria

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68
Q

NETs – Neutrophil Extracellular Traps

A

are made of processed chromatin bound to granular and selected cytoplasmic proteins which come from the lysed neutrophils

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69
Q

Pus

A

a mixture of dead bacteria and neutrophils

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70
Q

Link Innate and Adaptive Immunity

A

Antigen-presenting cells

via Antigen Presentation by Phagocytes

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71
Q

Specific/Adaptive immunity mediated by

A

Antibodies or cells

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72
Q

Humoral Specific/Adaptive Immunity

A

Antibody-Mediated
Immunity Involves the use of B cells
Transform into plasma cells and memory cells Synthesize and secrete antibodies

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73
Q

Involves the use of cytotoxic T cells

Kill infected body cells, cancer cells, foreign cells

A

Cell-Mediated Specific/Adaptive Immunity

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74
Q

Two molecular classes of MHC

A

MCHI

MCHii

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75
Q

chance of identical MHC

A

1 in 5 million `

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76
Q

Only people that have the same MHCs on their cells

A

identical twins

77
Q

MHC molecules structure

A

2 chains – alpha and beta

78
Q

MHC-I are on

A

all nucleated cells

79
Q

MHC-II are on

A

on all antigen-presenting cells

  • macrophages
  • dendritic cells
  • B cells
80
Q

antigen-presenting cell types

A

– Dendritic cell / Professional APC
– Macrophage
– B lymphocyte (B cell)

81
Q

Cells that have no MHCs on their surface

A

*erythrocytes have no MHCs on their surface

82
Q

T-cell receptors recognize

A

antigens only when they are associated with specific MHC proteins

83
Q

Antigen Presenting Cells (APCs) present

A

Exogenous Antigens with MHC-II

84
Q

Steps of Antigen Presenting Cells

A

STEPS:
• Ingest antigen
• Digestion into peptide fragments
• Synthesize and package MHC-II molecules
• Bind peptide fragments to MHC-II
• Insert antigen–MHC-II complexes on plasma
membrane

85
Q

Antigen

A

antibody generator

86
Q

Epitope

A

The part of the antigen that is recognized by the immune cells

87
Q

Characteristics of an antigen:

A

Reactivity - Antibody binds specifically to the antigen that provoked it
Immunogenicity - Ability to provoke an immune response by stimulating antibody production

88
Q

Adaptive Immune Response

A

Acquired, Specific

89
Q

Innate or Adaptive: Antigen (and epitope) specific

A

Adaptive Immune Response

90
Q

Innate or Adaptive: Antigen-presenting cells (APC) – (MHC-II + peptide)

A

Adaptive Immune Response

91
Q

Innate or Adaptive: The ability of the body to defend against specific microbes and foreign substances – Involves MEMORY for previously encountered antigens

A

Adaptive Immune Response

92
Q

Adaptive Immune Response Cells involved

A

B Cells and T Cells are involved

93
Q

Must recognize the specific foreign material to be attacked

A

B and T Lymphocytes

94
Q

Any molecule that can trigger an adaptive immune response against itself or the cell bearing

A

Antigen

95
Q

three stages of adaptive immune response

A

The encounter and recognition of an antigen by lymphocytes Lymphocyte activation
The attack launched by the activated lymphocytes and their secretions

96
Q

Origins of B Cells and T Cells

A

Bone marrow

97
Q

Where T cells mature

A

Thymus

98
Q

Where B cells mature

A

Bone marrow

99
Q

The first cell to show specificity

A

Helper T cell

100
Q

Co-Reception occurs between

A

B7 - CD28

101
Q

B7

A

on the antigen-presenting cell

102
Q

CD28

A

on T helper cell

103
Q

What results from the displacement of CD28 from B7 by CTLA4 and PD-1

A

Biological process that shut off the T cell activation

results in T cell inactivation

104
Q

Bacterial Infection leads to

A

antibody synthesis in secondary lymphoid organs

105
Q

Creates specific antibodies

A

Plasma Cells

106
Q

Macrophages and B cells Process and Present Antigen to a

A

Helper T cell

107
Q

CD4

A

co-receptor for the T-cell receptor

108
Q

Three Events Required for the Activation of Helper T Cells

A
  1. MHC-II + Peptide – TCR 2. Co-reception CD28 – B7 3. Cytokines from APC
    stimulate TH Cell
109
Q

B cells that secrete antibodies

A

Plasma cells

110
Q

B cells that are long-lived and are used for memory

A

Memory B cells

111
Q

Which plasma protein increases during infection

A

gamma globulins

112
Q

Antibody Structure

A

Contain four polypeptide chains
- Two Heavy chains that are Identical to each other
- Two Light chains that are Identical to each other
Flexible hinge region

113
Q

Variable region on an antibody

A

Antigen binding site

114
Q

Constant region on an antibody

A

Same in all antibodies of a class

115
Q

Types of antibody class:

A
  • IgG
  • IgA
  • IgM
  • IgD
  • IgE
116
Q

IgG

A

most common type of antibody

protect you against infection

117
Q

IgA

A

to protect the mucosal tissues from microbial invasion

118
Q

IgM

A

the largest antibody

first line of host defense against infections

119
Q

IgD

A

function unclear

120
Q

IgE

A

critical role in the allergic inflammatory process

allergic reactions

121
Q

____ cells will secrete specific antibodies

A

Plasma cells will secrete specific antibodies

122
Q

_____ cells which allow faster response if antigen is seen again

A

Memory cells which allow faster response if antigen is seen again

123
Q

B cells become activated in the _____

A

B cells become activated in spleen, lymphoid nodule, or lymph node

124
Q

B cells are activated in presence of

A

B cells become activated in the presence of a microbe

125
Q

Antibodies can be acquired actively/passively or both

A

Can be Actively or Passively Acquired

126
Q

Active Antibody Immunity

A

The person’s own immune system responds to microbe Long-lasting Protection – Memory Cells are involved

127
Q

Passive Antibody Immunity

A

The person receives antibodies from another person or animal Temporary Protection - NO Memory Cells are involved

128
Q

Active Natural Immunity

A

Develops when a person is exposed to an antigen by chance

129
Q

Active Artificial Immunity

A

Develops when a person is purposefully exposed to an antigen

130
Q

Passive Natural Immunity

A

IgG from mother to fetus across the placenta IgA in Breast milk

131
Q

Passive Artificial Immunity

A

Receive serum containing antibodies

From person or animal that has been vaccinated

132
Q

Flu virus

A

Active Natural

133
Q

Flu vaccine

A

Active Artificial

134
Q

A vaccine

A

may consist of small quantities of living or dead pathogens, small quantities of toxins, or harmless antigenic molecules derived from the microorganism or its toxin.

135
Q

Resistance built up as a result of the body’s contact with microorganisms, their toxins or other antigenic components (from an infection or vaccine)

A

Active Immunity

136
Q

The direct transfer of antibodies from one person to another

A

Passive Immunity

137
Q

antibody-synthesizing capacity of infants

A

relatively poor

138
Q

Antibody Functions

A

Antigen Neutralization Antigen Agglutination Antigen Precipitation Activating Complement Opsonization

139
Q

Neutralizing Antigen

A

Binding to bacterial toxins

140
Q

Agglutinating Antigen

A

Grouping of microbes with antigens

141
Q

Precipitating Antigen

A

Linkage of soluble antigen

142
Q

Activating Complement

A

Compliment protein becomes active when bound to antibody with microbe

143
Q

Activation of Classical Complement Pathway

A

C1 binds to antigen binding site, and the C3b on the bacterium binds to the phagocyte

144
Q

Opsonization

A

Direct Enhancement of Phagocytosis by Antibody

145
Q

Rate of Antibody Production Following Initial Exposure to an Antigen and Subsequent Exposure to the Same Antigen

A

At the second antigen exposure, the Antibody concentration is much greater

146
Q

Immune Memory Prevents

A

Disease

147
Q

CD8 cells

A

Cytotoxic T cells

148
Q

CD4 cells

A

Helper T cells

149
Q

Lymphocytes Must Gain

A

Immunocompetence - Develop Antigen Receptors

150
Q

Immunocompetence

A

Develop Antigen Receptors

151
Q

The body will/will not create antibodies to antigens on your own cells

A

Will NOT

152
Q

T helper cells are required to activate

A

B and Cytotoxic T cells

153
Q

Terminal deoxynucleotidyl Transferase

A

inserts N-nucleotides to J gene segment during rearrangements of genes
Increases specificity

154
Q

Antibody Classes is determined by

A

constant region

155
Q

Primary response by antibody (antibody type and concentration)

A

IgM initially and then IgG is produced

156
Q

Secondary response by antibody (antibody type and concentration)

A

IgM and IgG is produced, IgG is produced in a higher concentration

157
Q

Amplification is due to

A

production of memory cells

158
Q

T cells

A
  • Used in cell-mediated immunity to eliminate specific antigens
  • Require Activation - they are usually inactive
  • Become activated only when they bind to a foreign antigen
159
Q

T cells that don’t recognize MHC Class II molecules are of

A

no value and are negatively selected (the clone is destroyed)

160
Q

T cells that recognize MHC class II- self peptide complexes are

A

negatively selected (the clone is destroyed)

161
Q

Development of Immune Tolerance develops during

A

Immune tolerance develops during fetal and early postnatal life

162
Q

Immune tolerance develops due to

A

clonal deletion or clonal inactivation of cells that match body antigens

163
Q

Endogenous Antigen

A

Digestion of antigen – virus - into peptide fragments

164
Q

Steps of Infected Body Cells

A

Synthesis of MHC-I molecules
Binding of peptide fragments to MHC-I molecules.
Packaging of antigen–MHC-I complexes
Insertion of antigen–MHC-I complexes into the plasma membrane.

165
Q

Steps of Antigen Presenting Cells

A

Synthesis of MHC-II molecules
Binding of peptide fragments to MHC-II molecules.
Packaging of antigen–MHC-II complexes
Insertion of antigen–MHC-II complexes into the plasma membrane.

166
Q

Infected Cells Process and Present

A

Viral Antigens to a Cytotoxic T Cell

167
Q

Killing of Virus-Infected Cells is done by

A

Cytotoxic T cells

168
Q

Cytotoxic T cells release _______

A

perforin + granzymes

169
Q

perforin

A

perforin facilities entry of cytotoxic Granzymes into cell

170
Q

Granzymes

A

inducing apoptosis

virus cannot replicate and is released

171
Q

What does Antigen-MHC-I complex bind to

A

TCR

172
Q

Factors that Alter Resistance to Infection

A

• Protein–calorie malnutrition
worldwide, the greatest contributor to decreased resistance to infection
• Preexisting disease, infectious or noninfectious, can predispose the body to infection
• Stress and state of mind can enhance or reduce resistance to infection (and cancer)
• Modest exercise and physical conditioning have net beneficial effects on the immune system and on host resistance
• Sleep deprivation is associated with decreased immune function

173
Q

Immunodeficiency Diseases

A

Result from weak, underactive, or impaired immune systems

174
Q

𝑺𝑪𝑰𝑫 = 𝑺𝒆𝒗𝒆𝒓𝒆 𝑪𝒐𝒎𝒃𝒊𝒏𝒆𝒅 𝑰𝒎𝒎𝒖𝒏𝒐𝒅𝒆𝒇𝒊𝒄𝒊𝒆𝒏𝒄𝒚 𝑫𝒊𝒔𝒆𝒂𝒔𝒆

A

a group of related diseases that arise from an absence of both B and T cells and, in some cases, NK cells

175
Q

𝑨𝑰𝑫𝑺 = 𝑨𝒄𝒒𝒖𝒊𝒓𝒆𝒅 𝑰𝒎𝒎𝒖𝒏𝒐𝑫𝒆𝒇𝒊𝒄𝒊𝒆𝒏𝒄𝒚 𝑺𝒚𝒏𝒅𝒓𝒐𝒎𝒆 affects which cells

A

infects and kills helper T cells resulting in impaired immune responses to other infectious organisms.

176
Q

Harmful Immune Responses

A

Graft Rejection
Transfusion Reactions
Allergy (Hypersensitivity) Autoimmune Disease
Excessive Inflammatory Responses

177
Q

Tissue Grafts and Organ Transplantation

A

Class I MHC proteins on the graft cells and class II MHC proteins on the macrophages differ from the recipient

Consequently, the MHC proteins are recognized as foreign by the recipient’s T cells.

Cells bearing these proteins are destroyed by the recipient’s cytotoxic T cells with the aid of helper T cells.

Tools aimed at reducing graft rejection include radiation and drugs that kill actively dividing lymphocytes and thereby decrease the recipient’s T-cell population.

178
Q

cyclosporine

A

blocks the production of IL-2 and other cytokines by helper T cells. This eliminates a critical signal for proliferation of both the helper T cells and the cytotoxic T cells.

179
Q

Transfusion Reactions

A

illness caused when erythrocytes are destroyed during blood transfusion

180
Q

Antibody of A blood type

A

Anti-B

181
Q

Antibody of B blood type

A

Anti-A

182
Q

Antibody of AB blood type

A

Neither Anti-A nor Anti-B

183
Q

Antibody of O blood type

A

Both Anti-A and Anti-B

184
Q

Allergic Reactions

A

When a person is overly reactive to a substance that most others tolerate well

185
Q

Two types of allergic responses

A
  • Immediate Hypersensitivity

Delayed Hypersensitivity - Appears 12-72 hours after allergen exposure

186
Q

Anaphylaxis

A

large amounts of the chemicals released by the mast cells (or blood basophils) enter the circulation, systemic symptoms may result and cause severe hypotension and bronchiolar constriction.

187
Q

Autoimmune Disease

A

an inappropriate immune attack triggered by the body’s own proteins acting as antigens

The immune attack, mediated by autoantibodies and self-reactive T cells, is directed against the body cells that contain these proteins

188
Q

Autoimmune Disease Examples

A
  • Type 1 diabetes mellitus
  • Rheumatoid arthritis
  • Multiple sclerosis
  • Myasthenia gravis
189
Q

Autoimmune Disease Examples

A
  • Type 1 diabetes mellitus
  • Rheumatoid arthritis
  • Multiple sclerosis
  • Myasthenia gravis

PHGY 209 (10 decks)

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