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Physiology > Lecture 3/4: Immunology > Flashcards

Lecture 3/4: Immunology Flashcards

1
Q

Role of leukocytes

A

(aka white blood cells)

cells of the immune system that are involved in defending the body against both infectious and foreign materials.

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2
Q

Different types of leukocytes

A

Lymphocytes

Monocytes

Neutrophils

Eosinophils

Basophils

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3
Q

What happens to leukocytes when blood is centrifuged?

A

All leukocytes and platelets separate at the buffy coat

1% of blood sample

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4
Q

Two types of leukocytes

A

Granular leukocytes

Agranular leukocytes

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5
Q

How are granular leukocytes characterized?

A

by the presence of differently staining granules in their cytoplasm

e.g. neutrophils, eosinophils, basophils

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6
Q

How are agranular leukocytes characterized?

A

by the absence of granules in their cytoplasm

e.g. monocytes, macrophages, lymphocytes

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7
Q

What are lymphocytes?

A

A subset of agranular leukocytes that mediate innate and adaptive immunity

i.e. involved in immune response

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8
Q

Where are lymphocytes commonly found?

A

Lymphatic system

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9
Q

Cellular characteristics of lymphocytes

A

Deeply staining nucleus which may be eccentric in location

Relatively small amount of cytoplasm

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10
Q

Examples of lymphocytes

A

T cells

B cells

NK cells

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11
Q

% leukocytes in blood, descending order

A

Neutrophils (54-62), Lymphocytes (28-33), Monocytes (2-10), Eosinophil (1-6), Basophil (<1)

No macrophages and no dendritic cells present

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12
Q

What are neutrophils main function?

A

Bacteria, Fungi

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13
Q

What are basophils main function?

A

Release histamines for inflammatory responses

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14
Q

What are eosinophils main function?

A

Larger parasites

Allergic responses

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15
Q

What are lymphocytes main function?

A

B cells make antibodies

T cells regulate immunity to viruses, bacteria, cancer, autoimmunity

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16
Q

What are monocytes main function?

A

Phagocytic in blood stream.

Differentiate to macrophages in tissues

Majority found in spleen

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17
Q

What are macrophage main function?

A

Phagocytosis in tissues

Antigen processing and presentation

Not in blood

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18
Q

What are dendritic cell main function?

A

Antigen processing and presentation*

T cell activation*

Not in blood

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19
Q

Antigen definition

A

something that stimulates an immune response

Can be any molecule - components of pathogens, chemicals, self proteins, etc.

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20
Q

Antibody definition

A

a family of defensive proteins your body makes when it is stimulated by an antigen.

Antibodies contain sites that specifically bind one Ag and not another.

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21
Q

Lymphoid organ definition

A

Anatomical site where immune cells

and immune responses are generated

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22
Q

What are the two types of lymphoid organs?

A

Central or primary lymphoid organs

Peripheral or secondary lymphoid organs

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23
Q

Central or primary lymphoid organs

A

Sites of generation and education of lymphocytes (bone marrow, thymus)

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24
Q

Peripheral or secondary lymphoid organs

A

Sites where adaptive immune responses are initiated and where lymphocytes are maintained (eg. spleen, lymph nodes)

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25
Q

Essential characteristics of immune system

A

Highly specific: Adaptive is specific; innate is relatively non-specific

Self non-self discrimination (self recognition): Respond to foreign and tolerate self

A way of selectively amplifying particular immune responses

Diversity: converting one response into multiple effector types

Self Regulation: Turning responses off so that they don’t get out of control

Memory: Ability to remember previous encounter with same pathogen

Redundancy: Multipleback-ups,fail-safe mechanisms and alternatives

The ability to respond to a changing environment by inventing new Ag receptors: Highly polymorphic and endless combination of genetic segments for receptor coding

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26
Q

2 components of optimal immune response

A

Innate immunity

Adaptive immunity

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27
Q

Main function of innate immune system

A

A system that can respond virtually instantly to readily identifiable potential pathogens

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28
Q

Key characteristics of innate immunity

A

Constitutive

Quick to develop/initiate

Ag non-specific

Multiple effector mechanisms: both cell
-mediated and humoral components

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29
Q

Goal of innate immune system

A

Contain the pathogen in the initial hours and days of infection, giving more sophisticated defenses time to expand and be deployed.

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30
Q

Assets of innate immunity

A

Rapid (minutes to hours for full activation) , covers the 4-10 days needed for an adaptive immune response to develop

Intense (essential role in inducing a strong inflammatory response)

Natural Killer cells, eosinophils, basophils, macrophages, neutorphils, and dendritic cells

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31
Q

Main liabilities of innate immune system

A

No adaptability to new stimuli: hence no protection from novel pathogens (i.e. new flu variants)

No memory: no capacity to “learn from previous infections” (an innate immune response is the same speed, type and intensity on the first or 10th exposure to a pathogen)

Poor regulation: self/nonself discrimination not efficient resulting in collateral tissue damage

Poor amplification: Magnitude of response always same

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32
Q

How is innate immunity activated?

A

Activated by “danger signals” (molecules widely conserved on pathogens)

Pattern recognition receptors (toll like receptors - TLRs) on innate cells recognize Pathogen-associated molecular patterns (PAMPS)

Generation of inflammatory response (cytokines, chemokine, immune cell recruitment etc)

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33
Q

What is the trade off for “quick to respond to widely expressed danger signals that bind to a small family of receptors (~20)”

A

Absence of

Ag specificity

Specialization

Adaptability to new pathogens

Hence, we evolved an Ag-specific immune response!

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34
Q

What is adaptive immunity?

A

Specific host defenses that are mediated by B and T lymphocytes following exposure to antigens, and exhibit diversity and memory.

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35
Q

Key characteristics of specific immune response (adaptive)

A

Specificity: ability to recognize and respond to many different microbes

Memory: Enhanced responses to recurrent or persistent infections

Specialization: Responses to distinct microbes are optimized for defence against these microbes

Non reactivity to self antigens: prevents injurious immune responses against host cells and tissues

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36
Q

Two types of adaptive immunity

A

Cell-mediated immunity

Antibody-mediated Immunity

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37
Q

What is cell-mediated immunity conferred by?

A

T lymphocytes

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38
Q

Where do T cells develop?

A

Thymus

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39
Q

What molecule do all T cells express?

A

CD3

Also bear T cell receptor for antigen recognition

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40
Q

Helper T cell (molecule expressed, role, importance)

A

Express CD4 molecule

Help B cells to make certain classes (IgG and IgE) of Ab

Important for immunity to intracellular bacteria and parasites

Augmenting killer T cell response (cross priming reaction)

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41
Q

Killer or cytotoxic T cell (molecule expressed, role)

A

Express CD8 molecule

Important for killing viral infected and tumor cells

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42
Q

What does humeral immunity depend on?

A

Antibodies

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43
Q

Where do B lymphocytes originate and mature?

A

Bone marrow

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44
Q

What is the B cell receptor?

A

Membrane bound antibody

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45
Q

How does antibody production from B cells occur?

A

Ag binding triggers division, differentiation and antibody production

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46
Q

What are the progeny of B cells? How do they differentiate?

A

Plasma cells - differentiated from memory B cells, secrete Ab

Memory B cells - expanded B cells that carry specific Ag

T cells can stimulate B cells in spleen to differentiate

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47
Q

Which Ab is first produced in primary responses?

A

IgM

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48
Q

Role of IgM

A

Opsonization, activates complement, neutralizing Ab

The West Nile Virus antibody tests detect WNV- specific IgM. Presence of IgG alone means previous infection

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49
Q

Which Ab has highest concentration in serum?

A

IgG

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50
Q

Which Ab is transferred transplacentally?

A

IgG

important for fetal immunity and immunopathologies

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51
Q

Role of IgG

A

Dominates memory (secondary) responses in serum

Opsonization, activates complement, neutralizing Ab

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52
Q

Where is IgA found?

A

at mucosal surfaces (hence mediates
mucosal immunity)

In colostrum, tears, GI and respiratory secretions

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53
Q

Which is the major Ab at mucosal surfaces?

A

IgA

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54
Q

Role of IgA

A

Opsonization

activates complement

neutralizing Ab

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55
Q

Role of IgD

A

Who knows?

[may have a role in activating B cells]

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56
Q

Role of IgE

A

Parasite defense

mediate immediate type
hypersensitivity reactions

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57
Q

Relative abundance of IgE

A

~10,000x lower levels than IgG, even in allergic individuals

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58
Q

How antibodies work

A

Neutralization

Antibody-mediated cytolysis

Opsonization

Complement activation

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59
Q

Neutralization (Ab)

A

binding to toxins or pathogens block their interaction with cell receptor

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60
Q

Antibody-mediated cytolysis

A

binding of Ab couples pathogen to a cell with capacity to destroy pathogen

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61
Q

Opsonization (Ab)

A

Ab-coated particles are easier for phagocytes to ingest

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62
Q

Complement activation (Ab)

A

Leads to release of inflammatory mediators

63
Q

What is immunologic memory?

A

Ability of the immune system to respond more rapidly and effectively to pathogens that have been encountered previously

pre-existence of clonally expanded lymphocytes with specificity for that antigen.

Hallmark of adaptive immunity

64
Q

How is immunologic memory produced?

A

either by previous infection or by vaccination

65
Q

Schematic representation of memory response

A

See figure

66
Q

How do you tell different cell types apart?

A

Physical appearance

Clister of differentiation (CD) Ag system

67
Q

How is physical appearance used to tell different cells apart?

A

Lymphocytes small, granulocyte larger with granules that stain in different ways with dyes used in lab.

(Differential cell count)

68
Q

How is CD used to tell different cells apart?

A

~320 cell surface proteins (Ag) distinguished with Abs used as a diagnostic tool.

Allows us to positively identify different cell types, function, state of activation (~150 cell types).

69
Q

Where is CD3 found?

A

T cells

Not B cells

70
Q

Two main subgroups of T cells

A

CD4: helper T cells

CD8: cytotoxic T cells

71
Q

What CD markers are found on B cells but not T cells?

A

CD19

CD20

72
Q

Where is CD56 found?

A

is on NK cells but not other types of lymphocytes.

73
Q

How is self/non-self discrimination achieved?

A

Achieved by early and continuous presence of self-antigens

74
Q

What is self/non-self discrimiation? Importance?

A

Property of the adaptive immune system to recognize and mount specific/targeted responses to foreign antigens without responding to self

Important for self tolerance and control of autoimmunity

75
Q

What is self tolerance?

A

Ability to remain “tolerant” to self while retaining the capacity to mount response to non-self.

Self/non-self discrimination with in-built fail-safe mechanisms are key

76
Q

How do the innate and adaptive immune responses talk to each other?

A

See figure

77
Q

What is inflammation?

A

A “protective” cellular and vascular connective tissue reactions to injurious insults

Can be acute or chronic

78
Q

Major aims of inflammation

A

Dilute

Destroy

Isolate

Initiate repair

79
Q

Characteristics of inflammation

A

Redness

Hotness

Swelling

Pain

Loss of function

80
Q

What is acute inflammation?

A

Immediate and early response to tissue injury (physical, chemical, microbial, Immunologic, etc.)

81
Q

What happens during acute inflammation

A

Vasodilation: Accounts for warmth and redness

Vascular leakage and edema: Protein leakage increases interstitial osmotic pressure
contributing to edema (water and ions)

Leukocyte emigration (mostly PMNs): Leukocytes leave the vasculature to mediate phagocytosis, degranulation and tissue damage

82
Q

What are PMNs?

A

Polymorphonuclear cells

Other name for granulocytes

Due to varying shapes of nucleus

83
Q

Possible outcomes of acute inflammation

A

Complete resolution

Scarring (fibrosis)

Abscess formation occurs with some bacterial or fungal infections

Progression to chronic inflammation

84
Q

What occurs during complete resolution of acute inflammation

A

Little tissue damage (healing by first intention)

Tissue regeneration

85
Q

What occurs during scarring (fibrosis) as an outcome of acute inflammation

A

Healing by secondary intention) usually resulting from infections,
malnutrition and immunodeficiencies

Tissues are unable to regenerate

Excessive fibrin deposition organized into fibrous tissue

86
Q

What is chronic inflammation?

A

An inflammatory response of prolonged duration

weeks - months - years

87
Q

What is chronic inflammation provoked by?

A

persistence of the causative stimulus

88
Q

What occurs simultaneously with chronic inflammation?

A

presence of acute inflammation, tissue destruction and repair

89
Q

What are the possible causes of chronic inflammation?

A

Infectious organisms that resist clearance and form a persistent infection in tissue or undrained abscess cavities

Exposure to irritant non-living foreign material that can not be removed

Potentially normal tissue components as seen in auto-immune diseases

90
Q

Examples of infectious organisms that resist clearance and form a persistent infection in tissue or undrained abscess cavities

A

mycobacterium tuberculosis

actinomycetes

treponema palidum

Staph aureus (in bone and pleural cavities)

91
Q

Examples of exposure to irritant non-living foreign material that can not be removed

A

implanted materials into wounds (wood splinters)

inhaled materials (silica, asbestos)

deliberately introduced material (surgical suture material or prosthesis)

92
Q

Examples of normal tissue components as seen in auto-immune diseases

A

Beta islet cells in diabetes mellitus type I

Acetylcholine receptors in Myasthenia gravis

93
Q

Characteristics of chronic inflammation

A

Lymphocyte, macrophage, plasma cell (mononuclear cell) infiltration

Tissue destruction by inflammatory cells

Fibrosis and angiogenesis (new vessel formation), resulting from unsuccessful attempts at repair

94
Q

Outcome of chronic inflammation if not successfully repaired

A

Ulcers

Fistulas (ex: holes in stomach which can allow stomach acid to be released)

Granulomatous diseases (Chron’s, macrophages secrete substances that destroy tissues)

Fibrotic diseases (Scaring)

Adhesions (fibrotic masses, can block blood flow)

Cancer

combinations of the above

95
Q

What is active immunity?

A

Your immune system actively

participates in building/developing the immunity

96
Q

What is passive immunity?

A

Your immune system does not actively contribute to the development of the immunity.

It passively acquires it by transfer of pre-made immune effector molecules.

97
Q

Types of active immunity

A

Natural: Recovery from natural infection

Artificial: Deliberate exposure (vaccination)

98
Q

Advantages of active immunity

A

Stronger immunity

More diverse response (both humoral and cell-mediated)

Longer lasting (can last up to years; sometimes lifetime)

Memory develops

99
Q

Disadvantages of active immunity

A

Takes several weeks to months to fully mature

100
Q

Types of passive immunity

A

Natural: Transfer from mother to fetus (IgA and IgG)

Artificial: Injection of preformed immune molecules - Antibodies (antitoxins, antivenoms etc), immune cells

101
Q

Advantages of passive immunity

A

Intense response

Immediate protection

102
Q

Disadvantages of passive immunity

A

Short duration (rapid catabolism)

Development of allergic reactions (e.g. serum sickness)

No memory develops.

103
Q

What is a vaccine?

A

A preparation of microbial Ag, often combined with adjuvants, administered to elicit protective, memory immune response against the original pathogen

Can be based on attenuated or dead organism or subunits

104
Q

What is an adjuvant?

A

Substance added to a vaccine, which is unrelated to a vaccine

Starts mounting immune response before body detects Ag

105
Q

What is the rational of a vaccine?

A

Elicit immunity against molecules found on the virulent pathogen without the same degree of risk associated with genuine infection.

106
Q

What are killed vaccines?

A

Killed whole organism is used as vaccines

Polio, Hep A, rabies, diphtheria

107
Q

Advantages of killed vaccines

A

It doesn t cause disease

There is no chance of reverting to virulence

Very cheap to make

Can be used in immunocompromised patients

108
Q

Disadvantages of killed vaccines

A

Induce poor immunity (mostly antibody)

Immunity is not sustained (short duration)

Require booster immunizations

109
Q

What are genetically engineered and live-attenuated vaccines

A

virulence factor has been removed

Body has to continuously fight

Ex: measles, smallpox, yellow fever, chicken pox

110
Q

Advantages of genetically engineered and live-attenuated vaccines

A

They cause infection without pathology

Strong protection (humoral and cell-mediated)

Long-lasting immunity (due to memory)

Minimal booster immunization

111
Q

Disadvantages of genetically engineered and live-attenuated vaccines

A

There is the fear of reverting to virulence

Cannot be used in immunocompromised patients (body is already fighting something else off)

Cold-chain sequence (stability in developing countries?)

112
Q

What is a subunit vaccine?

A

Part of virus that is most antigenic is identified and used as vaccine

113
Q

Advantages of subunit vaccine

A

Increased safety

Less antigenic competition since only a few components are included
in the vaccine

Vaccines can be targeted to the site where immunity is required

Ability to differentiate vaccinated animals from infected animals (marker vaccines).

114
Q

Disadvantage of subunit vaccine

A

Generally require strong adjuvants

Duration of immunity is generally shorter than with live vaccines.

Peptide vaccines often need to be linked to carriers to enhance their immunogenicity

A pathogen can escape immune responses to a single epitope versus multiple epitope vaccines.

115
Q

Characteristics of a useful vaccine

A

Very safe: Effective protection without significant danger of causing the disease itself or side effects (relative risk: death rate due to disease vs death rate due to immunization)

Effective over long period to time

Stimulate development of the right kinds of immunity

Chemically stable

Relatively affordable (economics of production and administration)

116
Q

What is herd immunity?

A

Herd immunity is the phenomenon where non-immunized individuals can be protected by the fact that most of the population around them is immune

117
Q

Protective immunity vs. hypersensitivity

A

Protective immunity: Desirable reaction

Hypersensitivity: undesirable reaction. All are secondary/memory responses

118
Q

What are hypersensitivity diseases?

A

Excessive or aberrant immune response to foreign antigens

Deregulated or uncontrolled immune response

Immune response to foreign antigen may be directed to self
antigens

119
Q

Clinical and pathologic features of hypersensitivity disease are varied depending on

A

Nature of antigen

Type of immune response

Host genetics

120
Q

Gel and Coombs classification of hypersensitivity diseases

A

Type I - IgE ab

Type II - ab to tissue antigens

Type III - immune complexes

Type IV - cell mediated immunity

121
Q

What happens during a type I hypersensitivity reaction?

A

Immediate

Initial meeting with allergen causes no symptoms, but sensitizes a susceptible person, which causes IgE Abs to be secreted that attach to the surface of mast cells and basophils

Later encounters with same Ag causes an immediate reaction in which Ag binds and cross-links IgE antibodies on the surface of cells.

Leads to massive release of histamines and other preformed mediators

Vasodilation and smooth muscle contractions

122
Q

What is the most common type of allergy?

A

Type I

Virtually impossible to resolve

123
Q

Treatment of Type I

A

Treatment of symptoms

124
Q

Examples of Type I hypersensitivities

A

Allergic rhinitis

eczema

asthma

bee/wasp stings

drugs (e.g. penicillin, insulin)

food allergy (e.g. seafood and nuts)

125
Q

Worst case of Type I hypersensitivity

A

Anaphylaxis

Need epinephrine (epi pen)

126
Q

Clinical example of type I hypersensitivity

A

Penicillin skin tests detect IgE ! red bump right away your are allergic

127
Q

Other name for Type II hypersensitivity

A

Ab-dependent cytotoxic hypersensitivity

128
Q

Cause of Type II hypersensitivity

A

IgM/IgG binding to cell surface molecules results in usual effects: Complement activation, opsonization, RBC agglutination.

Abs specific for altered components of human cells: eg Penicillin adsorption on RBCs.

129
Q

Examples of type II hypersensitivity

A

Transfusion reactions

Hemolytic disease of the new born

Drug-induced hemolytic anemia

Certain autoimmune diseases (Rheumatic fever, Autoimmune anemias, thrombocytopenias)

130
Q

What happens during Type III hypersensitivity

A
  1. Ags are widely spread and antibodies (IgM and IgG) form insoluble immune complexes
  2. Complexes deposited in vessels
  3. Inflammation via complement activation. Damage to local tissues
131
Q

Examples of Type III hypersensitivity

A

Rheumatoid Arthritis

SLE (lupus).

132
Q

Other name for Type IV hypersensitivity

A

delayed-type hypersensitivity (DTH)

133
Q

Triggers of Type IV hypersensitivity

A

Poison ivy

cheap jewelry/reactive metals

bacteria (TB)

virus (Hepatitis B)…

134
Q

How are type IV hypersensitivities mediated?

A

T cells and their cytokines

Upon re-activation T cells secrete cytokines (that cause inflammation and kill (CTL), monocyte influx, swelling..

135
Q

What types of cells are found at the site of inflammation in type IV hypersensitivities

A

Although initiated by T cells, more than 90% of cells at site of inflammation are non-T cells

136
Q

Examples of Type IV hypersensitivities

A

Contact Dermatitis

Granulomas

Organ specific autoimmune diseases

137
Q

What type of hypersensitivity is the tuberculin skin test?

A

DTH

Inject Tuberculosis protein (Mycobaterium tuberculosis) into the inner
surface of forearm

after 72hrs if there is a red bump, the person has been exposed to TB

138
Q

Types of immunodeficiency

A

Congenital (primary) immunodeficiency

Acquired (secondary) immunodeficiency

139
Q

Congenital (primary) immunodeficiency

A

Defects in lymphocyte maturation

Defect in activation and function

Defects in innate immunity

140
Q

Acquired (secondary) immunodeficiency

A

HIV and AIDS

Malnutrition

Chemotherapy/irradiation

Cancer metastasis to bone marrow – Splenectomy

141
Q

Gene therapy for immunodeficiency diseases

A

replacement of defective gene in self- renewing precursor cells

Very distant goal

142
Q

Aims of current therapy for immunodeficiency

A

Minimize and control infections

Replace defective or absent component by adoptive transfer and/or transplantation

143
Q

Agents used in replacement therapy for immunodeficiency

A

Pooled gammaglobulins for agammaglobulinemic patients

Bone marrow transplant for Secondary imunedeficienty

Enzyme replacement therapy for adenosine deaminase (ADA) and purine nucleoside phophorylase (PNP) deficiencies seen commonly patients with common variable immunodeficiency syndrome

144
Q

How to treat secondary immunodeficiency

A

Control opportunistic infections

Treat primary cause

145
Q

What is autoimmunity?

A

Refers to failure of an organism to recognize its own constituent parts as self

Allows an immune response against self cells, organs and tissues

Tissue damage usually resulting from inflammatory responses

146
Q

What are the types of autoimmune disease

A
  1. Systemic Autoimmunity
  2. Organ-specific

See figure

147
Q

Systemic autoimmunity

A

Autoimmune diseases involving several organs and tissues

Most involve both humoral and cell-mediated
immunity

148
Q

Organ-specific autoimmunity

A

Immune response directed to specific organs leading to cellular damage and organ destruction

149
Q

Factors influencing autoimmune disease development

A

Genetic: HLA, FcgR, FAS/FASL, Complement proteins

Environmental: microbes

Gender: females greater than males (estrogen?)

Others: injury

150
Q

Treatment of autoimmune diseases

A

Conventional therapies

New therapies

Experimental therapies

151
Q

Conventional therapies for treatment of autoimmune diseases

A

Anti-inflammatory agents

Immunosuppressive agents

Lymphocyte specific Abs

152
Q

New therapies for treatment of autoimmune diseases

A

Blocking TNF receptor (e.g. Embrel)

Depletion of cells e.g. Rituximab (anti-CD20 mAb) to treat systemic lupus erythematosus (SLE) - B cells in SLE are hyper responsive

153
Q

Experimental therapies for treatment of autoimmune diseases

A

Induction of Tolerance

Blocking peptides

Physiology (19 decks)

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