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PMP-101 > Immune and Adaptive Immune System I : Antigen Recognition > Flashcards

Immune and Adaptive Immune System I : Antigen Recognition Flashcards

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1
Q

Immunity: two systems

A

1) Innate immunity / nonspecific resistance
2) adaptive immunity / specific immunity

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2
Q

Define Innate immunity

A

Response to pathogens same each time the body is exposed

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3
Q

Define Adaptive immunity

A

Response to pathogens improves each time the pathogen is encountered.
Characteristics: Specificity and memory

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4
Q

What is Specificity ?

A

Adaptive immunity: recognize a particular substance eg specific virus or bacteria

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5
Q

Memory
Links to what system?

A

Adaptive immune system: “remembers” previous encounters with a particular substance.
Future responses are faster, stronger, and longer-lasting

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6
Q

If pathogen is destroyed before any symptoms develop, the person is said to be ______.

A

immune

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7
Q

Innate Immunity

A
  • Rapid and non specific
    Consists of
    Physical Barriers
    Chemical Mediators
    Leukocytes (WBC)
    Inflammatory Response
  • Enhances adaptive immune response
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8
Q

List the Physical Barriers;

A

Skin
Epidermal Keratinized cells
Sweat and secretions – lower pH

Mouth / oral cavity
Salivary glands – lysozyme

Stomach/GI tract
Low pH

Mucosal epithelia
GI tract
Respiratory tract
Ears
Nose
Traps and removes

Tears, saliva, and urine wash these substances from body surfaces
Pathogens cannot cause a disease if they cannot get into the body

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9
Q

What are Chemical Mediators?

A

Promote the immune system

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10
Q

Chemical mediators - examples and how they work;

A

Complement
> 20 Proteins in plasma
Normally inactive
Once activated - series of reactions - each complement protein activates the next.

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11
Q

Chemical mediators - step by step process

A

Contribute to adaptive and innate systems
Innate: “alternate pathway” of complement activation

Bind to the cell membrane of the pathogen labelling it for phagocytosis (OPSONIZATION)

Act as chemotactic agents to attract phagocytic cells to the site of inflammation

Form damaging pores in the plasma membrane of the pathogen
Cells swell and lyse (rupture)

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12
Q

3 pathways - Chemical mediators
Wha is the most importnant?

A
  1. alternate pathway (Innate)
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13
Q

Other examples of chemical mediators;

A
  1. Cytokines
  2. Interferons (IFNs)
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14
Q

Cytokines;

A

is signaling molecule that allows cells to communicate with each other over short distances.

Cytokines are secreted into the intercellular space, and the action of the cytokine induces the receiving cell to change its physiology.

A chemokine is a soluble chemical mediator similar to cytokines except that its function is to attract cells (chemotaxis) from
longer distances.

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15
Q

Interferons

A

are proteins that protect the body against viral infections. When a
virus infects a cell, the infected cell produces viral nucleic acids and proteins, which are
assembled into new viruses. The new viruses are then released to infect other cells. Because
infected cells usually stop their normal functions or die during viral replication, viral
infections are clearly harmful to the body

Fortunately, viruses often stimulate infected cells to produce interferons, which do not protect the cell that produces them.
Instead, interferon bind to the surface of neighboring cells > stimulate those cells to produce antiviral proteins. In this way interferon is like a “Save yourself!” signal from an infected cell to its neighbors.
These antiviral proteins inhibit viral reproduction by preventing the production of
new viral nucleic acids and proteins.
Some interferons play a role in activating immune cells, such as macrophages and natural
killer cells (see “White Blood Cells” in this section).

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16
Q

Concise definition cytokines

A

Small signalling molecules released from cells to trigger immune response
Egs Interleukins + chemokines + interferons

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17
Q

Concise definition Interferons (IFNs)

A

Viruses:
Induce cells to produce viral nucleic acids and proteins

Cells infected with viruses secrete interferons
Travel to adjacent cells and induce them to make antiviral proteins

Prevents production of new viral nucleic acids and proteins
Inhibit viral reproduction in these surrounding cells

Some IFNs also activate other immune cells (macrophages and NK cells)

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18
Q

Chemical mediators;

A

Histamine
Prostaglandins
Leukotrienes

Variously;
vasodilation,
increasing vascular permeability
stimulating phagocytosis
Promote inflammation

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19
Q

Innate Immunity: White Blood cells
[Production + release + type of cell]

A

> Produced in red bone marrow / lymphatic tissue

> Chemicals released from pathogens or damaged tissues attract WBC
Leave blood and enter tissue

> Phagocytic cells
Neutrophils normally first
Release signals that increase inflammatory response
Recruits and activates other immune cells
Pus- dead neutrophils
Macrophages (monocytes that leave blood)
Larger - later stages of an infection
cleaning up dead neutrophils and other cellular debris

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20
Q

Innate immunity - inflammatory cells

A

Inflammatory cells
Basophils
Mobile cells
Mast cells
Non mobile cells in connective tissue
Eosinophils
Allergic response
When activated: release histamine and leukotrienes
 Inflammatory response

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21
Q

Natural Killer cells

A

NK cells recognize classes of cells, eg tumour cells / virus-infected cells

Kill their target cells
releasing chemicals that damage cell membranes –> causes the cells to lyse

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22
Q

Inflammatory Response

A

Hallmark of the innate immune

Tissue injury (eg bacterial infection causing damage)
Mast cells/ basophils degranulate

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23
Q

What does the inflammatory response release > chemical mediators???

A

Stimulates releases or activation of chemical mediators
- Histamines
- Prostaglandins
- Leukotrienes
- Complement

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24
Q

Process which happpens in the inflammatory respone

A

Vasodilation (particularly histamine / prostaglandin)
Dilation of local capillaries
Increased blood flow (brings WBC / phagocytes)
Heat / redness

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25
Q

Characteristics of inflammatory response;

A

1) Increased vascular permeability (histamine)
leakage of fluid into tissue > swelling /oedema
Allows complement to enter tissue
enhances inflammatory response / attracts more phagocytes
Clotting factors enter (fibringogen- fibrin) –
Wall off/ first step in wound repair

2) Recruitment of phagocytes (Leukotrienes / complement)
Phagocytes leave blood and enter tissue
Neutrophils
Followed by macrophages

3) Cycle continues until the pathogens are destroyed

4) Phagocytes remove microorganisms and dead tissue
damaged tissues are repaired.

26
Q

Is the inflammatory response; local + systemic

A

Local:
Redness, heat, swelling, pain

Systemic:
More widespread
More neutrophils
Pyrogens > fever – hypothalamus
In severe cases: Sepsis - decreased blood volume can cause shock and death

27
Q

Adaptive immune response

A

Specificity and Memory

Antigens:
substances that stimulate adaptive immune responses
Foreign (bacteria, viruses, pollen, food)
Self (tumour)

Adaptive Immunity
Antibody Mediated / Humoral Immunity
Protein generated by plasma cells
differentiated B cell

Cell-mediated
T cells
Helper T cells (Th)
Cytotoxic T cells

28
Q

Lymphocyte: Origins
Where do they originate?

A

= from stem cells in Red Bone Marrow
>B cells mature in in bone marrow
>T cells mature in thymus

29
Q

Clones: Small no’s of identical B cells or T cells
form during embryonic development (and after)
Type any info about clones

A

Each clone derived from a single, unique B or T cell
Respond only to a particular antigen
> large variety of clones
> Antigen receptors on surface
- B-cell receptors
- T-cell receptors

> Each receptor binds with only a specific >antigen

Each lymphocyte clone have identical antigen receptors on their

Clones against self antigens normally eliminated

30
Q

Adaptive immune response - step by step

A

1) Antigen recognition by lymphocytes
Activates

2) Lymphocyte receptors and antigens combine
B cell and T cell receptors

3) Proliferation of lymphocytes recognising that antigen

31
Q

Antigens?
[bound to which molecule]

A

May be part of larger molecules
Eg after phagocytosis and b/d by macrophages
Bound to major histocompatibility complex molecules (MHC) on cell surface

32
Q

Recognition: MHC molecules
[classes]

A

Antigens presented by MHC receptors

MHC class I molecules
All other cells with nuclei
MHC class II molecules
APC – macrophages, dendritic cells lymphocytes (B and T cells)

Combined MHC and antigen can then bind to the antigen receptor on a B cell or T cell

Co-stimulation
Cytokines
Surface proteins

33
Q

Recap - innate immune system

A

> Non-specific
Physical barriers
Chemical Mediators
Leukocytes (WBC)
Inflammatory Response

> Hallmark: Inflammatory Response
Tissue injury –>
Vasodilation
Increased vascular permeability
Recruitment of phagocytes
Local or systemic

34
Q

Recap - Adaptive immune system

A

> Specific: Specificity and Memory
Antibody mediated
Cell mediated

> Lymphocytes need to recognise be activated by antigen
After pathogen phagocytosed antigen presented on surface of a cell (eg macrophage) by MHC molecule

> Lymphocyte clones proliferate

35
Q

What is not affected by antibodies?

A

Viruses

36
Q

Lymphocyte proliferation

A

> Helper T cells
MHC class II molecule
Macrophages release IL (helps to stimulate helper T cells)
Helper T cells
CD4 molecule

> Helps T cell receptor and MHC II molecule bind
After presentation: Helper T cells secretes IL2 stimulates them to bind

Helper T cells: ‘help’ B cells and other T cells to be activated

37
Q

Lymphocyte proliferation - can daughter cells divide again?

A

Yes, if presented with antigen

38
Q

Lymphocyte Proliferation - BC

A

Phagocytoses same antigen as Helper T cell

Presented on surface of B cell by MHC class II molecule

T-cell receptor binds to MHC class II / antigen complex
Aided/co-stimulated by CD4 molecule
Co-stimulated by ILs (TH cell)

Stimulate B cell to divide

These can go onto divide
Some will differentiate into Plasma cells
Produce Antibodies

39
Q

Antibody (Humoral) Immunity - Antibodies

A

Bind to antigens: destroyed
Extracellular antigens

40
Q

Antibody (Humoral) Immunity - Proteins

A

Y-shaped molecules
consisting of four polypeptide chains: two identical heavy chains and two identical light chains
Variable region (top)
Antigen binding site
Constant regions
Immunoglobulins (Ig)
IgG, IgM, IgA, IgE, IgD

41
Q

Antibody Production - primary response

A

First exposure to antigen
B cell undergoes several divisions

Forms plasma cells and memory B cells

Plasma cells produce antibodies

Normally takes 3–14 days

Normally develops disease symptoms

pathogen has had time to cause tissue damage

After antigen destroyed antibodies degrade and plasma cells die

IgM

42
Q

Antibody Production - secondary response

A

Previously exposed to antigen

Memory B cells quickly divide to form plasma cells

Quickly produce antibody

Makes more memory cells

Quicker to produce antibodies

More plasma cells/antibodies

Memory cells persist for long time
IgG

43
Q

What are the effects of antibodies?

A

Extracellular Pathogens

a) Inactivate antigen: antibody binds to an antigen or when many antigens are bound together

b) Activates Complement Cascade: Antigen binds to antibody. Antibody can then activate complement proteins > inflammation, attracts WBC and lyses cells

c) Initiates release of inflammatory mediators: Antibody binds to mast cell /basophil. Triggers degranulation

d) Facilitate Phagocytosis: Antibody binds to antigen. Macrophages attaches to Fc of the antibody and phagocytoses both the antibody and the antigen

e) Antibody dependent cellular activity : Activates cytotoxic cell responses. Cytotoxic cells release chemicals that destroy the antibody-bound antigen

44
Q

Antibodies (Immunoglobulins)

A

1) IgG
secondary immune responses
Some maternal IgGs cross the placental membrane

2) IgA
external secretions
saliva, tears, intestinal and bronchial mucus, breast milk

3) IgE
target gut parasites and are associated with allergic responses

4) IgM
primary immune responses

5) IgD

45
Q

Cell mediated Immunity

A

> Cytotoxic T cells
- Intracellular effects
pathogens, allergic reactions, tumours
- Essential Viral infections
- Antibodies can’t cross into cell
- Destroys infected/affected cell

46
Q

Proliferation Cytotoxic T cells - e.g. of virus

A

Viruses infect cells
Some viral proteins are broken down and become processed antigens
Combined with MHC class I molecules
displayed on the surface of the infected

47
Q

Proliferation Cytotoxic T cells - activation

A

T-cell receptors binding with the MHC class I/antigen with the MHC class I/antigen complex

48
Q

Proliferation Cytotoxic T cells
- co stimulation

A

surface molecule CD8

Helper cells: co-stimulation with eg IL2

Stimulates T cell to divide

49
Q

Cell mediated Immunity

A

> Series of divisions

> Additional cytotoxic T cells
Immediate response

> memory T cells
Secondary response
long-lasting immunity

50
Q

Cell mediated Immunity - Cytotoxic T cell Function

A

Release cytokines
Attract innate immune cells
Macrophages
Phagocytosis of antigen/cell
inflammatory response
Activate additional cytotoxic T cells

51
Q

Cell mediated Immunity - Directly kill virus infected cells

A

Viral antigens on surface
T cells bind to the antigens on the surfaces and cause the cells to lyse or under go apoptosis

52
Q

Cytotoxic T Cells Cytotoxic T (TC) cells _______ + _______
cells that display MHC-I-antigen complexes

A

attack + destroy

53
Q

Flow chart: Acquired ADAPTIVE immunity

ACTIVE

A

Level 1
Active immunity = immunity is provided by individual’s own immune system

Level 2
Natural = antigens are introduced through natural exposure
Artifficial = Antigens are deliberately introduced in a vaccine

54
Q

low chart: Acquired ADAPTIVE immunity

PASSIVE

A

1) Passive immunity = immunity is transferred from another person or an animal

2) Natural = antibodies from the mother are transferred to the child across the placenta or in milk

Artificial = antibodies produced by another person or an animal injected

55
Q

Allergic response

A

Immune response to a non-pathogenic antigen

Allergen is an antigen that is typically not harmful to the body

Sensitive individuals : inappropriate immune response

Sensitivity / hypersensitivity to the antigen

Immediate hypersensitivity reactions are mediated by antibodies

Sensitisation and Re-exposure Phase

56
Q

What is the Sensitization phase

A

equivalent to the primary immune response

57
Q

Allergic response

A

Antibodies Produced
IgE and IgG

IgE antibodies: immediately bound to mast cells and basophils.
Memory T and memory B cells formed

58
Q

Allergic response - Re-exposure

A
  • Allergen binds to IgE already present on mast cells
  • triggers immediate release of histamine, cytokines, other mediators
  • —> cause allergic symptoms
  • strong and rapid response
59
Q

What happens to an Aging Immune system?

A

> Little effect on the lymphatic system
remove fluid from tissues,
absorb lipids from the digestive tract
remove defective red blood cells

60
Q

Aging immune system - severe effect?

A

Severe impact on the immune system =
thymus replaced with adipose tissue
lose the ability to produce mature T cells
May lose functionality

Antigen exposure leads to fewer helper t cells
Less stimulation of B and cytotoxic T cells

61
Q

Aging immune system - responses?

A

Antibody and cell mediated responses decrease
Primary and secondary antibody responses decrease

62
Q

Aging immune system - responses?

A

Antibody and cell mediated responses decrease
Primary and secondary antibody responses decrease

PMP-101 (53 decks)

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