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Bellas Biology > Topic 6.3 Response to Infection > Flashcards

Topic 6.3 Response to Infection Flashcards

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1
Q

Leucocytes

A
  • White blood cells
  • There are two types:

Granulocytes- contain granules
-neutrophil
-eosinophil
-basophil

Agranulocytes- do not contain granules
-lymphocyte
-monocyte

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2
Q

Non-specific responses

A
  • Physical, chemical and mechanical barriers are non-specific (innate immunity- born with).
  • They attempt to prevent entry of all pathogens.
  • Some are part of biological responses in the blood, such as inflammation.
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3
Q

Inflammation

A
  • Activates the second line of defence.
  • Leucocytes (such as macrophages, neutrophils and the compliment system) are drawn to the infected area:
    -fight and eliminate the pathogen
    -initiate tissue repair
    —> Inflammation causes fever, heat and swelling often during infections- its often a sign the immune system is working.
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4
Q

Fever

A
  • Normal body temperature is around 37°C.
  • When infected by a pathogen, the hypothalamus raises your body temperature which inhibits bacterial growth.
  • Prolonged temperatures above 40°C can be damaging to your tissues and extensive water loss can be deadly.
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5
Q

Compliment System

A
  • Involves a number of proteins produced in the liver.
  • They target and coat invading pathogens.
  • Triggers inflammation which recruits extra immune cells to the area.
  • Extra immune cells carry out phagocytosis and kill the pathogens.
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6
Q

Cells of the Innate Immune System: Mast Cell

A
  • Cells involved in allergic responses, releasing histamine and other inflammatory molecules.
  • Sit within skin and muscle tissue.
    (Activate when come into contact with foreign antigens).
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7
Q

Cells of the Innate Immune System: Natural Kill (NK) Cell

A
  • Kill pathogen-infected cells and cancer cells.
  • Release chemicals called cytokines, which alert and attract other immune cells.
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8
Q

Cells of the Innate Immune System: Macrophage

A

Antigen Presenting Cells that destroy foreign substances by phagocytosis (engulfing them) and activate other immune cells.

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9
Q

Cells of the Innate Immune System: Neutrophil

A

Fast-acting phagocytes that flock to the site of inflammation.

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10
Q

Cells of the Innate Immune System: Basophil

A
  • Involved in allergic and inflammatory responses.
  • Releases histamine like mast cells (but unlike mast cells they circulate the blood).
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11
Q

Cells of the Innate Immune System: Dendritic Cell

A

Phagocytic Antigen Presenting Cells with and important role in altering T cells to new pathogens.

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12
Q

Cells of the Innate Immune System: Eosinophil

A

Phagocytes that also produce enzymes to counteract inflammatory molecules released by mast cells.

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13
Q

Cells of the Innate Immune System: Complement

A
  • A set of around 30 proteins in the blood plasma that can be activated by the presence of microbes or antibody-antigen complexes.
  • Can destroy pathogens and activate phagocytic cells.
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14
Q

The Non-Specific Immune Response

A

The non-specific immune response aims to stop any pathogens getting in regardless of what they are.
(Cells such as neutrophils or macrophages are non-specific).

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15
Q

The specific Immune Response

A
  • A specific response of the immune system to the pathogens.
  • Each T cell and B cell is tailored toward a specific pathogen and is not effective against any others.
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16
Q

Four Key Features of a Specific Immune Response

A
  • It can distinguish self form non-self.
  • It is specific to each foreign in cell.
  • It is diverse- can recognise potentially any foreign antigen.
  • Immunological memory- the secondary response to a pathogen is rapid.
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17
Q

Humoral Response

A
  • Humoral: bodily fluid.
  • The immune response to pathogens (and their antigens) free in the tissues and bloodstream.
    —> Involves specific antibodies
    1) Complimentary TH lymphocytes bind to foreign antigen on antigen-presenting T cells.
    2) Release cytokines that stimulate clonal expansion (rapid mitosis) of complementary B lymphocytes.
    3) B cells secrete antibodies with complementary variable region to antigen.
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18
Q

Cell Mediated Response

A
  • The response to your own body cells that have altered self-antigen.
    (eg. cells that have become infected by a virus, or have become -cancerous).
    1) Complementary TH lymphocytes bind to foreign antigen on APC.
    2) Stimulates:
    -Clonal expansion of complementary TH cells (rapid mitosis): become memory cells or trigger humeral response.
    -Clonal expansion of cytotoxic T cells: secrete enzyme perforin to destroy infected cells.
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19
Q

MHC

A
  • MHC: Major Histocompatibility Complex
  • A molecule found on the surface membrane of all cells and is used to present antigens, both self and non-self.
    —> MHC molecule in the membrane of a normal cell presents ‘self-antigen’ and leave these cells alone.
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20
Q

Antigen Presenting Cell

A
  • The phagocytic cells are known as antigen presenting cells.
  • After they engulf and digest pathogens they will present parts of the pathogen (antigens) on their surface attach to MHC molecules.
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21
Q

How do Antigen Presenting Cells work?

A
  • Phagocytic cells (eg. macrophages) engulf and digest pathogens.
  • They then present antigens of these pathogens on their surface.
  • Antigens are presented to T cells and their T cell receptors; this then activates those cells.
  • Activated T cells divide by mitosis, creating many more identical copies of each specific cell T cell.
22
Q

How do Helper T Cells work?

A
  • T cells are made in bone marrow, but mature in the thymus gland (hence ‘T’).
  • Each different helper T cell has a unique T cell receptor on its surface that fits a specific antigen.
  • T cells can only recognise antigen presented to them on MHC from antigen presenting cells.
  • Activated T cells divide rapidly mitosis, creating many clones.
  • These helper cells will activate other cells in the cell mediated response.
    -Develop memory cells
    -Stimulate phagocytes
    -Stimulate B cells
23
Q

Plasma B Cell (definition)

A

Short lived cells whose main function is to produce large amounts of antibodies against a particular antigen.

24
Q

Helper T cell (CD4+) (definition)

A

They help to activate:
- B cells to secrete antibodies.
- Macrophages to destroy microbes.
- Cytotoxic T cells to kill infected target cells.

25
Q

Memory B Cell (definition)

A
  • Mainly involved in the secondary response.
  • They rapidly differentiate into plasma B cells (and divide rapidly by mitosis) in order to quickly produce antibodies against the pathogen.
26
Q

Cytotoxic T cell (CD8+) (definition)

A

Effector cells that destroy virus-infected cells, etc that exist in the cytosol, or contiguous nuclear compartment.

27
Q

Antibodies (definition)

A

Antibodies can combine with viruses and toxins of pathogens to block them from entering or damaging cells.

28
Q

Antigens (definition)

A

Proteins on the surface of cells which trigger an immune response.
They are specific to particular cells.

29
Q

Perforins (definition)

A

They bind to the cell surface membrane of the target cell and pierce holes (perforate) in the membrane.

30
Q

B Cells Explanation

A
  • B cells are made and matured in the bone marrow (hence ‘B’).
  • Mature B cells circulate in the bloodstream and are concentrated in the lymph glands where lymph fluid drains back into the blood.
    —>They produce antibodies that target specific pathogens.
31
Q

What do B cells produce?

A
  • Antibodies.
  • These can be attached to the B cell plasma membrane, or released free into the cell.
32
Q

Steps in humeral response (?)

A

1) Clonal Selection: Activation of specific B cell with complimentary antibodies to the pathogens antigen.
2) Clonal Expansion: Mitosis (proliferation) so more cells have correct antibodies.
3) Differentiation: Plasma cells, B Memory cells.

33
Q

Antibodies explanation

A

As antibodies recognise antigens outside of cell, B cells and antibodies are involved in the humoral response.
1) Agglutination: When the antibodies bind to the antigens on the pathogen.
2) Opsonisation: When a pathogen is marked for phagocytosis. A chemical which makes an antigen or pathogen more recognised by phagocytes.
3) Neutralisation: Antibodies bind to and neutralise/inactivate viruses and toxins.

34
Q

B Cell Activation

A

Before B cells can produce their antibodies on mass, they must become activated.

35
Q

T Cell Independent Activation: Activation without the T cells

A
  • A B cell and its membrane-bound antibodies recognises and attaches to antigens.
  • The B cell becomes activated, divides by mitosis and produces antibodies.
36
Q

T Cell Dependent Activation: Activation with T cells

A

1) A B cell antibody receptor matches with it s complimentary antigen. A B cell internalised the antigen and presents it on its surface (like APCs).
2) An activated T cell (by the same pathogen) binds to the B cell, via this presented antigen.
3) The T cell produces cytokines which activate the B cell. After activation, the B cell divides by mitosis to produce memory B cells and B effectors cells. B effectors cells eventually differentiate into antibody producing plasma cells.

37
Q

Killer T Cells (cytotoxic- CD8+) Explanation

A
  • Activated in a very similar way to Helper T cells (cytokines from activated T Helper cells are required).
  • They can attack body cells which have been anti-genetically altered by viruses or cancer cells.
    -They destroy the pathogen by punching holes through their cell surface membranes so the cell contents spill out (lysis).
38
Q

Killer T Cell Activation

A

1) An APC (eg. macrophage) digests and engulfs the pathogen and presents the antigen on its surface via MHC.
2) Killer T cell with complimentary T cell receptors bind to the antigen on the APC.
3) Killer T cells becomes activated by release of cytokines from activated helper T cells (Killer T Memory cells are also formed).
4) Active T killer cells release perforin chemicals. These punch holes in the membrane of infected cells and cause them to burst (lysis).

39
Q

Primary Response

A

(First exposure to antigen: vaccine, infection)
—>Slow, weak
- Helper T cells activated
- Cause lysis
- B cells activated and divide
- Form plasma cells
- Produce antibodies
- Memory B+T cells left behind

40
Q

Secondary Response

A

(second exposure to antigen: long interval between primary + secondary)
—> Quicker, stronger
- Use of memory cells
- No symptoms
- Shorter time lag between exposure and antibody production
- Pathogen usually destroyed before any symptoms

41
Q

Passive immunity

A

When antibodies are introduced from outside the body; you don’t have to make them yourself.

42
Q

Artificial Passive Immunity

A

Can be used if there isn’t a vaccine ready yet or if someone requires a tetanus injection or requires antibodies for a snakebite.

43
Q

Artificial Passive Immunity: Advantage

A

Immediate- don’t need to wait for antibodies to be made.

44
Q

Artificial Passive Immunity: Disadvantage

A

Short term- the person will not have a long lasting protection.

45
Q

Natural Passive Immunity

A

An example is when an infant receives a mothers antibodies through the placenta or breast milk.

46
Q

Active Immunity

A

Active immunity involves exposure to a pathogen/antigen.
-Either though natural exposure (natural active)
-Or through vaccination (artificial active)

47
Q

Vaccination

A

Vaccination aims to stimulate a primary immune response, without actually causing the disease like a normal infection would.
This allows people to safely develop memory cells against a pathogen.
1) Vaccine contains dead/inactive form of a pathogen or antigen
2) Triggers primary immune response
3) Memory are produced and remain in the bloodstream, so secondary response is rapid & produced higher concentration of antibodies
4) Pathogen os destroyed before it causes symptoms.

48
Q

Phagocytosis (version 2- better)

A

1) Phagocyte moves towards pathogen via chemotaxis.
2) Phagocyte engulfs pathogen via endocytosis to form a phagosome.
3) Phagosome fuses with lysosome (phagolysosome).
4) Lysozymes digest pathogen.
5) Phagocyte absorbs the products from pathogen hydrolysis.
(Antigen presenting occurs at end).

49
Q

How do antibodies lead to the destruction of a pathogen?

A
  • Formation of antigen-antibody complex results in agglutination.
  • Activation of complement.
  • Opsonisation (marks microbes for phagocytes).
  • Precipitation/ neutralisation (makes toxins insoluble).
50
Q

Examples of passive and active immunity

A
  • Passive natural: antibodies in breast milk/ across placenta.
  • Passive artificial: anti-venom, needle stick injections.
  • Active natural: humeral response to infection.
  • Active artificial: vaccination.

Bellas Biology (34 decks)

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