Chapter 12 Immune Response Flashcards

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1
Q

What is the primary defence to prevent pathogens entering?

A

Skin as a barrier of entry, with healthy bacteria on the surface to limit space, and sebum to inhibit pathogen growth
Mucous membranes, goblet cells to produce mucus, trapped bacteria, steeped to stomach acid or lysozymes or phagocytes to kill
Expulsive refluxes in vomiting and diarrhoea to clear contents of guts, sneezing and coughing to eject mucus
Blood clotting

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2
Q

What is the basic process of blood clotting?

A

When platelets come in contact with proteins such as collagen, they trigger blood clotting
Platelet release clotting factors e.g thromboplastin
Thromboplastin with Ca2+ catalyses Thrombin to prothrombin, Fibrin to fibrinogen, insoluble so forms the mesh
Platelets also release serotonin to cause narrowing of damaged blood vessels

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3
Q

What is and what causes inflammation?

A

Localise pain, heat and redness
Caused by mast cells that are activated in damaged tissue, which secrete histamines to dilate blood vessels and increase blood plasma leakage
Also release cytokines to attract phagocytes

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4
Q

What causes fevers and how does it help the immune system?

A

Stimulated by cytokines from mast cells, targeting the hypothalamus
Increasing body temperature reduces pathogen reproduction and they prefer cooler temperatures
Also increases the speed of the specific immune system

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5
Q

Define phagocytosis

A

The process of phagocytes engulfing and destroying pathogens

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6
Q

Explain the process of phagocytosis

A

1) Pathogens secrete chemicals that attract phagocytes
2) Phagocytes recognise non-human proteins, recognises as non self
3) Phagocytes engulf pathogen, enclosing it in a vacuole called the phagosome via endocytosis
4) Phagosome fuses with a lysosome to form a phagolysosome
5) Hydrolytic enzymes in the phagolysosome destroy the pathogen
6) If a macrophage, the antigens from the pathogen combine with glycoproteins called major histocompatability complex (MHC), to move antigens to the cell surface, become an antigen presenting cell, APC, which triggers the specific immune system
7) These then secrete cytokines which attract more phagocytes and T/B lymphocytes

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7
Q

What is the difference between neutrophils and macrophages?

A

Neutrophils are phagocytes with a multi lobed nucleus which increases space for lysosomes, and helps the neutrophil squeeze through space, pathogens destroyed only
Macrophages are also phagocytes with a more round nucleus, which can become APCs when the antigens from a pathogen fuse the MHC glycoproteins

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8
Q

What do phagocytes release after engulfing a pathogen?

A

Cytokines, cell signalling molecules which attract more phagocytes and also increased body temperatures

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9
Q

What is an opsonin?

A

Compounds that bind to the antigen of a pathogen, which also bind to receptors in phagocytes
So makes it easier for phagocytes to identify and bind to pathogens

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10
Q

Describe the structure of antibodies

A

They contain a light chain bonded to a heavy chain via disulphide bridges, with two of these complexes per antibody
They contain a variable region which is specific to each antibody and the antigen they bind two, each antibody can bind to two antigens, and a constant region
They have a hinge region to more easily bind to two antigens, and a binding site to other receptors- provides flexibility
Antigens and antibodies form antigen-antibody complexes

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11
Q

How do antibodies help the fight against pathogens?

A

Acts as an opsonin, so flagged to phagocytes
Agglutinin- causes agglutination, binding of multiple antibody-antigen complexes to more easily remove pathogens, prevents spread of pathogens
Antitoxins, Binds to toxins to neutralise them
Prevents pathogens from invading more host cells

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12
Q

What is the process of cell mediated response?

A

1) A T helper cell with receptors complementary to the antigen binds to the APC, activating the T cell.
2) They secrete interleukins, which stimulate B cells and macrophages, but also allow the T cell to undergo mitosis and differentiation to become:
-T helper cells
-T killer, secrete perforin to make holes on pathogen cell membrane
-T regulator, suppresses immune system
-T memory, remembers antigen

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13
Q

What is the process of humoral immunity?

A

1) B cells with receptors complimentary to the antigens of a pathogen bind to the antigen and engulf it. They became an antigen presenting cell.
2) An activated T-helper cell with receptors complimentary to the antigen binds to the antigen on the B cell APC. This binding is called clonal selection.
3) The T-helper cell now produces interleukins which activate the B cell.
4) Clonal Expansion then takes place. The activated B cell will proliferate into B plasma cells which release antibodies complementary for the antigens, and B memory cells that remain circulating in the blood.

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14
Q

When is humoral immunity used? When is cell mediated immunity used?

A

Cell Mediated respond to cells which have been changed in some way, such as viruses and cancer- as they can secrete perforin and kill these cells
Humoral responds to antigens found outside cells, for fungi and bacteria as they release antibodies

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15
Q

What are auto immune diseases? Give an example

A

A disease where the immune system attacks healthy body tissues, respond to body cells antigens
E.g Rheumatoid Arthritis, attacks joints
E.g Type 1 Diabetes, Attacks pancreas

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16
Q

What is active and passive immunity?

A

Active- body makes antigens
Passive- body given antigens, not created by the body

17
Q

What is artificial and natural immunity?

A

Artificial- controlled by humans, does not occur without human interference
Natural- happens naturally

18
Q

Give examples of active, passive, natural and artificial immunity

A

Vaccination- active, artificial
Breastfeeding passing antibodies- natural passive
Normal encounter with virus- natural active
Vaccinations for rabies- give antibodies in injection, artificial passive

19
Q

How do memory cells helped with secondary response? How do second dose vaccines work?

A

If a B memory cell finds an antigen it corresponds to, triggers division, very quickly produced plasma cells

Second dose vaccines work because the level of b memory fall low, but on second exposure, they will proliferate and increase in number again

20
Q

How do vaccines work?

A

1) Pathogen made safe by killing it, weakened strain, toxins modified, purely antigens, or genetically engineered
2) Small amounts injected into the blood
3) Primary immune response triggered, produce memory cells
4) If come in contact again, quick response as memory cells quickly proliferate into B plasma and T killer or other Ts to enhance cytotoxic effect- kill pathogen

21
Q

How can genes/environment affect someone’s immune response?

A

Genes determine the type of glycoprotein receptors synthesised in t/b cells, which bind to antigens
So genes can determine whether specific immune response to a certain pathogen can occur
And so if antibodies can be produced
Mutations can lead to new antibodies being synthesised, or new MHC alleles

Environment can cause autoimmune disease if pathogen similar shape
Vaccinations
Naturally encounter with pathogen, memory cells
Diet and speed of immune response
Nature effecting epigenetics

22
Q

What does the antibody concentration look like after being vaccinated and encountering the pathogen again?

A

Antibody concentration has a sharper rise and a much higher peak
The level stays higher than the previous peak as memory

23
Q

What would a lack of B cells cause?

A

A greater susceptability to pathogens/infections (not necessarily disease as whole)
As antibodies cannot form