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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
Characteristics of inflammatory response;
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
Is the inflammatory response; local + systemic
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
Adaptive immune response
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
Lymphocyte: Origins Where do they originate?
= from stem cells in Red Bone Marrow >B cells mature in in bone marrow >T cells mature in thymus
29
Clones: Small no's of identical B cells or T cells form during embryonic development (and after) Type any info about clones
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
Adaptive immune response - step by step
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
Antigens? [bound to which molecule]
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
Recognition: MHC molecules [classes]
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
Recap - innate immune system
> 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
Recap - Adaptive immune system
> 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
What is not affected by antibodies?
Viruses
36
Lymphocyte proliferation
> 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
Lymphocyte proliferation - can daughter cells divide again?
Yes, if presented with antigen
38
Lymphocyte Proliferation - BC
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
Antibody (Humoral) Immunity - Antibodies
Bind to antigens: destroyed Extracellular antigens
40
Antibody (Humoral) Immunity - Proteins
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
Antibody Production - primary response
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
Antibody Production - secondary response
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
What are the effects of antibodies?
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
Antibodies (Immunoglobulins)
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
Cell mediated Immunity
> Cytotoxic T cells - Intracellular effects pathogens, allergic reactions, tumours - Essential Viral infections - Antibodies can’t cross into cell - Destroys infected/affected cell
46
Proliferation Cytotoxic T cells - e.g. of virus
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
Proliferation Cytotoxic T cells - activation
T-cell receptors binding with the MHC class I/antigen with the MHC class I/antigen complex
48
Proliferation Cytotoxic T cells - co stimulation
surface molecule CD8 Helper cells: co-stimulation with eg IL2 Stimulates T cell to divide
49
Cell mediated Immunity
>Series of divisions >Additional cytotoxic T cells Immediate response >memory T cells Secondary response long-lasting immunity
50
Cell mediated Immunity - Cytotoxic T cell Function
Release cytokines Attract innate immune cells Macrophages Phagocytosis of antigen/cell inflammatory response Activate additional cytotoxic T cells
51
Cell mediated Immunity - Directly kill virus infected cells
Viral antigens on surface T cells bind to the antigens on the surfaces and cause the cells to lyse or under go apoptosis
52
Cytotoxic T Cells Cytotoxic T (TC) cells _______ + _______ cells that display MHC-I-antigen complexes
attack + destroy
53
Flow chart: Acquired ADAPTIVE immunity ACTIVE
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
low chart: Acquired ADAPTIVE immunity PASSIVE
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
Allergic response
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
What is the Sensitization phase
equivalent to the primary immune response
57
Allergic response
Antibodies Produced IgE and IgG IgE antibodies: immediately bound to mast cells and basophils. Memory T and memory B cells formed
58
Allergic response - Re-exposure
- 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
What happens to an Aging Immune system?
> Little effect on the lymphatic system remove fluid from tissues, absorb lipids from the digestive tract remove defective red blood cells
60
Aging immune system - severe effect?
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
Aging immune system - responses?
Antibody and cell mediated responses decrease Primary and secondary antibody responses decrease
62
Aging immune system - responses?
Antibody and cell mediated responses decrease Primary and secondary antibody responses decrease

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