Chapter 7 and 8: Immunity Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Antigens

A

markers on the surface of cells, they are proteins, so they must be transcripted and translated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Self Antigens

A

they can identify and recognise the cells of your body, so the immune system doesnt attack its own cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Non-Self Antigens

A

The immune system reads these antigens as foreign meaning they get attacked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MHC Class I Markers

A

all cells with a nucleus in the body xpress MCH Class I markers,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MHC Class II Markers

A

found on specialised cells within the immune system, antigen presenting cells so they can present the pathogen to the T helper cells, the B cells and the cytotoxic T cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathogen

A

an agent that causes a disease and merits and immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Self and Non-Self receptors

A

B and T cells have these receptors on the surface that recognise the antigens as self or nonself `

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Autoimmune diseases

A

when the immune system attacks against its own cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Alergies

A

the response is initiated by the body recognising an antigen as non-self, which it launches a strong immune response too, the allergen isnt pathogenic and cannot cause the body harm, only the immune response can

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

First line of defence

A
  • innate immune system
  • physical barrier
  • chemical barrier
  • microbiological barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

1st line of defence - Plants - Physical

A

thick bark, waxy cuticles of the leaves, formaltion of galls, presence of thorns and trichomes, ability to close and open the stomata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

1st line of defence - Plants - Chemical

A

Chitinase, phenolds, defensins, saponins, oxalicacid and glucanases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

1st line of defence - Animals - Physical

A

Intact skin
mucose secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

1st line of defence - Animals - Chemical

A

lysosome in tears and saliva
acidic sweat
stomach acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

1st line of defence - Animals - Microbiological

A

bacteria on the skin, lower gastro intestinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Second line of defene

A

non specific
happens simultaneously with the 3rd line of defence
faights all pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Innate

A
  • non specific
  • quick response
  • no memory
  • short lived
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Phagocytes

A

macrophage, dentritic cells, neutrophils
- non specific (eats everything)
- they engulf and destroy extracellular pathogens
- cleases cytokines wich help singal other cells about the pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Phagocytosis

A
  1. phagocytes recognise (by antigens and receptor) the pathogens and engulf it
  2. the pathogen is enclosed in a vesicle called a phagosome, before it fuses with a lysosome, which releases lysozymes that break down the pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Natural Killer Cells

A

eliminated intracellular pathogens
- undergoes degranulation, induces apoptosis
- large granulated cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

e

degranulation

A
  1. NK needs to identify the viral infected cells
  2. releases granzyme which are a type of protease to break down proteins
  3. perforin is releases to create pores on the surface of the plasma membrane f the infected cells
  4. granzyme enters the infected cells
  5. inducing apoptosis (controled cells death) via the intracellular pathway the mitochondrial pathways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

NK - Killer inhibitory receptor

A

examines cells for MHC class I markers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

NK - Killer activation receptor

A

binds to molecules on cells that are undergoing cellular stress
- KAR can be stoped if the KIr detects a sufficient amount of MHC Class I markers, if the KIR cant bind to MHC Class I markers then cell death occurs through degranulation

24
Q

Antigen presenting cells

A

macrophages and the dendritic cells, destroy pathogen but then display them on their surface, MHC Class II

25
Q

Mast Cells

A
  • live in connective tissue
  • when they detect injury they become activiated and degranulate, releasing histamine, which is important in the inflammatory response.
  • histamine which stimulates the vasodilation and increases permiability of the blood vessels
26
Q

eosinophils

A

contain toxins that help destroy invading pathogens, like DNases and RNases, they area white blood cell and they often are involved with allergic reactions and asthma

27
Q

interferons

A

it releases a type of cytokine called interferon, which tells the nearby cells to undergo changes so they can protect themselves against pathogens
- they stop protein production in cells
- they increase the number of enzymes that destroy RNA

28
Q

Complement proteins

A

They are proteins that form the complement system, they activate eachother in a process called the complemnt cascade.

  1. opsonisation - CP coat the pathogen which allows the immune system to recognise it as foreign (more tastey)
  2. chemotaxis -they gather aroud the pathogen leading the immune cells towards it so then it can be destroyed
  3. lysis - CP joig together on the surface of the pathogen creating a membrane attack complex which will create a pore in the membrane of the cell which mean fluid rushes in and the cell will lyse.
29
Q

lymphatic system functions

A
  • transportation of apc to 2nd lymphoid tissue
  • produces leukkocytes
  • removal of fluid around the body
  • ## absorbtion of fatty acids
30
Q

Inflammation

A
  1. initiation - someting damages the skin, and introduces pathogens, the macropahges in the tissue are activated and they release cytokins, mast cells deganualte releasting histamine
  2. vasodilation - histamine induces vasodilation and increases permeability of the blood vessels, cells from the immune system can now enter the infection site
  3. migration - phagocytes and complement proteins arrive guided by cytokines released by damaged cells and activated macrophages, where the phagocytes engulf and destroy pathogens aided by the complement proteins.
31
Q

Primary Lymphatic tissue

A
  • creates and matures lymphocytes
  • bone marrow and thymus
32
Q

Secondary lymphatic tissue

A
  • maintain lymphocytes
  • they maintain lymphocyes and activate the adaptive immune response
  • lymph nodes and spleen
    -
33
Q

Lymphatic transport

A
  1. Lymphatic drainage - collects fluid from the inflammatory response, via the lymphatic capillaries which are very small and collectect fluids and pathogens, this fluid is now called lymph where it is carried eventually toward the lymthnode
  2. lymphatic flow - the lympohatic cappillaries joing together and form larger vessels. they rely on muscle movements to sqeeze lmyph through the system, the heart is not responsible, it travels in one direction, away from tissues toward lymph nodes
  3. Lymphatic surveilence - Afferent tissues takes the lymph through the clusters of b and t cells, as it drains the aps and pathogens will meet a lymphocyte with the complementary receptors, if this happens the efferent vessels will take antibodies away from the lymph nodes, where it will be curculated around the body by the heart.

THIS IS WHY THERE IS A DELAY IN THE ADAPTIVE IMMUNE RESONSE

34
Q

clonal selections

A

selection of cells, so the b cells will recognise the pathogen and then they get reproduces via clonal expansion

35
Q

clonal expansion

A

the b cells clones itself with the help of t-helper cells which release cytokines to help the b cells expland quicker, they both recognise the same pathogen

36
Q

differentiation

A

the cells split into plasma cells which produce antibodies and them b memory cells which are stored for later

37
Q

Antibodies

A
  • molecule (they dont kill pathogen)
  • the place where the antigens bind to the antibody is called the variable region or antigen binding site
  • heavy chain (big big)
  • Light chain (small small on the outside)
  • help together by disulphide bonds
  • control extracellular pathogens
38
Q

antibodies function

A
  1. opsonisation - cover the pathogen and make it more suseptible to the actins of phagocytes
  2. actives complement proteins
  3. neutrilisation - they block the section on a pathogen where they need to get into the cells they also bind to the active site of toxins where they stop it from causing harm
  4. Agglutination - antibodies can bind to 2 antigens on 2 seperate pathogens meaning a large antigen-antibopdy complex is formed where it becomes immoblised and allows for easier recognition as a pathogen for phagocytes.
39
Q

T - helper cells

A
  • lymphocyte
  • produced in bone marrow and matured in the thymus
  • they active b cells and cytotoxic t cells
  • they are activated just from the antigen presenting cells.
40
Q

B - Cells

A
  • extracellular
  • produced and matured in the bone marrow
  • they can recognise a pathogen directly on the pathogen, from an antigen presenting cells or from free floating antigens
41
Q

cytotoxic t cells

A
  • intracellular
  • activeted by the t helper cells by the cytokins
  • act the same as NK cells
  • release granzymes and perforin throuigh degranulation, which induces apoptosis of the infected cell
  • they are specific they destroy specific pathogens
  • they are a product of clonal selection from t cells which differentiaate into t memry cells and cytotoxic t cells
42
Q

vaccines

A

attenuated - still live but weak
inactivated - the virus is like dead
subunits - small sections of the virus like an antigen
dna/rna - sections of the dna/rna that contain genetic information

43
Q

herd

herd immunity

A

95% of population need to be vacinated for effective herd immunity
eldery and young people cannot be vaccinated becuase of their weakend immune systems

44
Q

virulence

A

the potential of a pathogen or disease to cause serious illness or harm

45
Q

acti

activation

A

induced immune system

46
Q

supression

A

prevent immune system

47
Q

Monoclonal Antibodies

A
  1. identify and isolate the antigen you want the monoclonal antibodies to bind to (supress or activate)
  2. vaccinate the mouse with the antigen
  3. the mouse will undergo clonal selection and expansion of the b cells
  4. extract the b cells from the spleen of the mice
  5. fuse the b cells with myeloma cells (which allows them to replicate more quickly) this is called a hybridoma
  6. screen and select for the cells with the correct antibodies,
  7. they are then cloned
  8. they are then purified and collected for use for a patient (these are monoclonal antibodies)
48
Q

Immunotherapy (antibody therapy)

A

Monoclonal Antibodies
- less side effect
- designed in labs
- they bind to specific cells

49
Q

Naked monocloal antibodies

A

just antibody by its self, no drugs or radioactive material
- they bind to antigen on cnacer cells and act as a marker (tag), which attracts immune cells, signalling them to destroy this cell as now they recognise it almost like a non-self antigen
- they interfere with the growth and development of tumors, by binding to the chemical releases by cancer cells so the growth is stoped byneutralising these chemicals, they block the activation of growth factors

50
Q

Conjugated monoclonal antibodies

A
  • a monoclonal antibody that has been joined with a chemotheraphy drug or radioactive prticles
  • the monoclonal antibodies bind to the surface of the cancer cell and they deliver drugs or the radio active material and then the drug destroys the cell.
51
Q

Antigens

A

Antigens are molecules that interact with the immune system, in that
they provoke some kind of immune response.

52
Q
A
53
Q

IgD

A

important for the activation of other immune cells

54
Q

IgE

A

responsible for allergic reactions

55
Q

spleen b cells?

A

only b-plasma cells

56
Q

monoclonal antibodies symptoms

A
  1. they are foreign so they could possible cause an allergic reaction
  2. they induce an immune response so then the the immune system starts an attack which can cause symptoms