Immunity

Question 1

What is immunity?

Answer 1

Protection against diseases.

Question 2

What is the immune system

Answer 2

The body’s defense system

Question 3

What are our bodies line of defense against diseases?

Answer 3

Our body has its own line of defense against diseases to prevent infectious diseases from entering and spreading.

1) First line of defense
* External, non-specific
For example saliva (antibacterial enzymes), tears (antibacteria enzymes), stomach acid (low pH kills harmfull substances).
2) Second line of defense
* Internal, non-specific immune response
* Involves phagocytes
3)Third line of defense
* Internal, specific immune response
* involves lymphocytes

Both non-specific and specific defenses work together to protect the body against disease.

Question 4

Define antigens

Answer 4

Two types:
Self and non self antigens
In general, antigens are macromolecules on cell surfaces
E.G protein, glycoprotein,glycolipid, polysachharides etc.

1) Non self-antigen=macromolecules that activates an immune response
* Macromolecules are found on…
-foreigh materials surface e.eg pathogen, allergen
-surface membrane of infected host cell
🡢Stimulates production of antibodies

2) Self antigens/cell marker
* Macromolecules on cell surface membranes of host cells
* Cell surface antigens do NOT trigger body’s immune system.
* No antibodies are produced.

When we say antigen in genral we usually mean non self antigen.

Question 5

Define immune response

Answer 5

Immune repsonse is the body’s immune reaction towards non-self antigens.

Involves WBCs that made in bone marrow

1) Phagocytes
(mostly non-specific defence)
* Neutrophils
* Monocytes
🡢which mature into macrophages

2) Lymphocytes
(mostly specific defence)
* B-lymphocytes
* T-lymphocytes

Question 6

Describe phagocytes

Answer 6

• Produced throughout life
  Function:
• Patrol in blood, tissues and organs
• remove dead cells and pathogens
• By Phagocytosis (chap 4)
• involved in non-specific defense
  🡢responds to many different non-self antigens

Appearence:
Lobed nuclei
Granular cytoplasm-due to many vesciles

e.g. Neutrophils
* Multi-lobed nucleus
* Have receptor proteins on its membrane
🡢To identify pathogens as non-self

• When there is an infection, large numbers are released from bone marrow.
• Accumualte at site of infection
• Short-lived (few hours-days)
• Dies after digesting pathogens.
• Dead neutrophils form pus.

Question 8

Describe the structure of monocytes

Answer 8

Phagocytes
Monocyte🡢Macrophage
* Lobed nucleus/Kidney-bean shaped
* Larger than neutrophils
* Have receptor proteins on its membrane
🡢To identify pathogens as non-self

• Monocytes=circulate in blood
• Mature into macrophages when it leaves blood and enters organs.

Long lived cells
Macrophages found in organs such as liver, lungs, spleen, kidney and lymph nodes.

Question 9

What is the role of macrophages?

Answer 9

Starts the immune response:

Mechanism:
1) Has various receptor proteins
* Can identify non-self antigens
* non-specific

2) Engulf pathogen/foreign material via phagocytosis
* fusion of phagocytic vacoule with lysosome

3+4) Cuts up pathogen using lysozomes

5) Antigens presented on its cell surface.
🡢Macrophages act as antigen presenting cells (APC)

6) Some cell fragments releases by exocytosis
* Antigen presenting cells can activate/stimulate lymphocytes.

Question 10

Describe lymphocytes.

Answer 10

Produced in bone marrow before birth
* involved in specific immune responses
🡢Responds to only specific non-self antigens
* Mature lymphocytes circulate in the blood and lymph
* Accumulate at sight of infection.

2 main types:
* Smaller than phagocytes
* Large round nucleus
* Little cytoplasm

there are two main types:
Both made in bone marrow, but mture in different places and have different functions.

1. B-lymphocytes (B cells)
   * Mature in bone marrow
   * Produce Antibodies
2. T-Lymphocytes (T cells)
   * Mature in thymus
   * does NOT produce antibodies.

Question 11

How many types of lymphocytes are there?

Answer 11

There any millions of different types of B and T lymphocytes with receptors of different shapes.So the body can respond to almost any type of pathogen.

However lymphocytes are SPECIFIC=each types of lymphocyte responds to 1 type of antigen only. For e.g. each type of B cell produce 1 type of antibody receptor.
🡢which responds to 1 type of antigen only.

Question 12

Describe maturation of B lymphocytes.

Answer 12

1) All B cells are formed in the bone-marrow before birth.
🡢Genes in B cells that code for antibodies code for diff types of antibodies for diff types of B cells.

2) Forms a specific antibody that acts as glycoprotein receptor on surface membrane of B cells.
🡢The specific antibody receptor will bind to specific antigen that is complementary in shape.

3) B lymphocytes divides and mature in bone marrow.
🡢Mature B lymphocytes circulate in blood and concentrate in liver, spleen and lymph nodes.

Question 13

describe antibodies.

Answer 13

Antibodies are also known as immunoglobins.
They are globular proteins (carbo part is not usually shown in diagram).
Made of four polypeptide chains:
2 heavy chains
2 light chains
🡢Quaternary structure
Held together by disulphide bonds.

Question 14

Describe the first region of antibodies.

Answer 14

There are three regions:
Variable region (Fab)
* Formed by light and heavy chains
* Provide 2 indentical antigen-binding sites.
* Specific for binding antigen
🡢Complementary shape to antigen
🡢Shape determined by primary structure
=Specific sequence of amino acids.
* R groups at antigen-binding site forms H bonds and ionic bonds with specific antigen.

Sequence of amino acids at the variable region is different for each type of antibody.
🡢Each type of antibody binds to different antigens.

Question 15

Describe the second region of antibodies?

Answer 15

2) Constant region (Fc)
* Formed from light and heavy chains
* When antibodies circulating in blood: they bind to receptors on phagocytes
* When antibody acts as B cell receptor: constant region attches to cell surface membrane of B cell.
* Constant region gives antibodies class.

Question 16

Describe the third region of antibodies.

Answer 16

3) Hinge region
* Held by disulphide bridges
* Gives flexibility when binding to antigen

Question 17

What are the 6 actions of antibodies?

Answer 17

1.Prevent entry into cell
2. Attach to flagella
3. Agglutination
4. Lysis of pathogen
5. Opsonisation
6. Neutralise toxins (antibodies also acts as antitoxins)

Question 18

Describe how antibodies prevent entry into cell and how the antibodies attach to flagella?

Answer 18

Antibodies combine with viruses and bacterial toxins preventing them entering or damaging cells.
Antibodies attach to flagella of bacteria making them less active and easier for phagocytes to engulf.

Question 19

Describe how antibodies cause agglutination and lysis of pathogen?

Answer 19

Antibodes with multiple antigen binding sites cause agglutination (clumping together) of bacteria recucing the chances of spread throughout the body.
Together with other molecules, some antibodies “punch” holes in the cell walls of bacteria, casuing them to burst when they absorb water by osmosis.

Question 20

Describe how antibodies cause opsonisation and neutralise toxins.

Answer 20

Antibodies coat bacteria, making it easier for phagocytes to ingest them, phagocytes have receptor proteins for heavy polypeptide chains of antibodies.
Antibodies combine with toxins, neutralising them and making them harmless, these antibodies are called antitoxins.

Question 21

Describe the action of B lymphocytes after maturation.

Answer 21

1. Pathogens Invade
2. Antigen presentation cell formation
3. Only specific B lymphocytes has receptors with the complementary shape to antigen will be activated
   →Clonal selection
4. B cell divides by mitosis
   →Clonal expansion
5. Activated B cells develop into plasma cells and memory cells.

Question 22

Describe plasma cells

Answer 22

• Short lived (few weeks)
• Produce and secrete antibodies rapidly by exocytosis into blood plasma, lymph, lungs and stomach lining.
• Antibodies are glycoproteins.
• So plasma cells have extensive have extensive network of RER and golgi.

Question 23

Describe memory cells

Answer 23

• Long lived and remain in circulation in blood and lymph.
• Provide long term immunity
• Last for many years/lifetime
• Enable faster response durig 2nd invasion of the same antigen, as many memory cells are circulating.
• During 2nd invasion of the same pathogen, it divides rapidly (clonal expansion).
  →Form more plasma cells→more antibodies
  →Infection is destroyed before symptoms develop.
  →Body immune to pathogen.

Question 24

Analyse the graph of concentration of antibody vs time in memory cells.

Answer 24

1st exposure to Antigens:
Primary response:
* Slower response
* Only a few B cells specific to the antigen is present
* Induvidual becomes ill.

2nd exposure to antigen:
Secondary response:
* Faster response
* Many memory cells circulating
* More cells specific for pathogen, higher chance of encountering pathogens quickly,
* More plasma cells formed
* More antibodies produced
* No symptoms developed.

Question 25

Describe the maturation of T-lymphocytes.

Answer 25

1) All T cells are produced in bone marrow before birth
2) Maturation in thumus gland
→Thymus shrinks after puberty
* Produce specific T cell receptors on cell surface membrane.
→Binds to specific antigen that is complementary in shape
→T cell receptor’s structure similar to antibodies (not antibody reeptors).
3) Mature T cells circulate in blood and lymph.

Question 26

Describe the action of T-Lymphocytes after maturation.

Answer 26

1. Pathogens invade.
2. Antigen presentation cell formation.
3. Only specific T lymphocytes has receptors with the complementary shape to antigen will be activated.
   →Clonal Selection.
4. T cell divides by mitosis.
   →Clonal expansion.
5. Activated T cells develop into T helper cells and T killer cells.

Question 27

What are the functions of T helper cells?

Answer 27

1) Secrete cytokines/interlukins which…
A) Stimulate specific B cells
* to divide and develop into plasma cells and memory B cells
* Increased antibody levels
B) Stimulate macrophages
* to carry out phagoytosis more rapidly
c) Stimulate Killer T cells
* to divide and produce more toxins

2) Form T helper memory cells
* Secondary repsonse
* Long term immunity

Question 28

What are the functions of cytotoxic T killer cells.

Answer 28

1) Seeks out infected host cells (including APC, cancer cells) and pathogens and destroys them.
a) attach to surface of cells
b) “punches” holes into cells
c) secrete toxins into cells .g. hydrogen perxoide or perforin.
2) Forms killer T memory cells
* Secondary responses
* Long term immunity as it is long lived.

Question 29

Give a summary of the immune response

this is what to write when asked for description of immune response

Answer 29

1) Pahogocytes engulfs antigen which produces antigen presenting cell.
2) APC presents the antigen to lymphocytes activating humoral (antibody-mediated) immune response or the cell meidated immune response.
3) The humoral immune response is concerning B cells which develop into plasma cells which produces antibodies and memory B cells which are in charge of long term immunity.
4) The cell mediated immune repsonse is involving T cells. The activated T cells will produce T killer cells which secrete toxins into infected host cells which will kill it or produce T helper cells which secrete cytokines. T helper cells will develop T helper memory cells and T killer cells will develop into T memory killer cells.

There are three types of memory cells.

Question 30

What are the types of immunity?

Answer 30

Active: Own immune response is activated.
-Own lymphocytes are activated by antigens
-Own antibodies are made
-Takes time not immediate
-Memory cells formed→Results in long term immunity.
e.g. Natural: Infection
Artificial:Vaccination

Passive: Immune response is NOT activated.
-Own lymphocytes are not activated.
-No plasma cells to produce antibodies.
-Protection is immediate
-No memory cells are produced.
e.g. natural: Maternal antibodies
Artificial: monoclonal antibodies.

Question 31

How does the immune response work together?

Answer 31

Antibodies bind to antigens and present to pahgocytes so that they can englulf them more. B cells activated by APC can also become an APC. Cytokines also help (we already studies their role in previous flashcard).

Question 32

Describe active natural immunity

Answer 32

E.G: Catching a cold
Natural: Antigens from the enviroment

Question 33

Describe active artificial immunity

Answer 33

E.G: Vaccination

Artificial: Antigens are introduced via injection into vein or muscle/consumed
Antigen used could be dead or alive.
→Activate the immune response artificially
Antigens can be attenuated/made hearmless (e.g. heat-treated, cut up, inactivated toxins).

Question 34

Describe passive natural immunity.

Answer 34

An example is maternal antibodies.

Natural:
1) Antibodies pass from mother to infant through placenta.
→Remain for months

2) Breast milk that is colostrum rich has antibody (lgA-Immunoglobin A) that prevents growth of bacteria/viruses in the stomach of infant.

Question 35

Describe passive artificial immunity.

Answer 35

Injection of antibodies or antitoxins.

Artificial: Antigens are introduced via injection.

Antibodies are collected from blood of donor/animals who are vaccinated or suffer from the same disease.

Contains the specific antibodies against the specific antigen.

Question 36

Describe the graph of active natural antibodies.

same graph as memory antibodies.

Answer 36

The first hump is due to the primary response.
Only a few B cells specific to the antigen is present.
Induvidual becomes ill.

The second hump is due to the secondary response.
It is a faster response,
many memory cells circulating.
more cells specific for pathogen, higher chance of encountering pathogens quickly
More plasma cells are formed
More antibodies are produced.
No symptoms developed.

Question 37

Describe the graph of passive natural immunity.

Answer 37

Concentration of antibody in blood of fetus or infant vs time after conception.

The concentration increases until birth after which it drops.
this is because maternal antibody passed from placenta to fetus drops in concentration after birth. protection is temporary.

Looks like a triangle.

Question 38

Describe the graph of passive artificial immunity.

Answer 38

Concentration of antibody in the blood vs time. (time after first and second infection).

Concentration of antibody increases immediately but decreases over time. Only provides short term protection.
Only way to get immediate immunity is to take injection again.

Question 39

Describe effective vaccines.

Answer 39

Provide sufficient antigens
→To mimic or copy natural infections.
→To form sufficient plasma and memory cells for long-term protection.

Give lifetime protection against pathogen.
→Pathogen unable to develop in immunised person.

For example vaccines using live pathigens for example small pox vaccines.

Question 40

Describe ineffective vaccines

Answer 40

Do not mimic natural infection
→No plasma and memory cells formed

Do not give lifetime protection
→Require booster injections
→to stimulate secondary response in order to give protection.

Do not provide sufficient protection against pathogen.
→Maybe due to pathogen’s high mutation ratr or ability to hide from immune system.

For e.g. vaccines using dead pathogens, cholera vaccine.

Question 41

What are the two modes of vaccination?

Answer 41

Mass Vaccination: Vaccinate a large number of people at the same time.
Ring Vaccination: Perform contact tracing with infected person. vaccinate the area of community the person is in/people who was in contact with the person.

Aim: Vaccinate a high porportion of the population. →To acheive herd immunity.

Question 42

Describe herd immunity

Answer 42

• Mass vaccination results in herd immunity.
• less chance of transmission of disease.
  →Reduce pool of infected people in the community.
  →Fewer people can catch the disease and be source of infection.
• Protection of those unvaccinated/immunocompromised as disease does not spread.

Question 43

What are the common barriers to vaccination?

Answer 43

1) Poor response to vaccine
* People that are immunocompromised (HIV, Old or Young Children).
* People who lack protein (malnutrition)
* Less antibodies made (antibodies are glycoproteins).
2) pathogens can mutate rapidly (antigenic variation)
* Form different starins with different antigens.
* Memory cells are unable to recognise pathogen that has major changes in antigen structure.
3) Pathogens can escape from immune system (antigenic concealment)
* By living inside cells/covering bodies with host proteins/supressing immune system.

Question 44

How was smallpox eradicated?

Answer 44

An effective vaccine was developed!!

• Same vaccine used everywhere.
  Varioloa virus-stable, low mutation rate.
• Use live virus so strong immune response → Similar to vaccinia virus.
• One doese enought to give life-long immunity, no boosters needed,
• Vaccine is heat stable.
• Easy to administer.
  → use bifurcated needle
  →Needle can be steralized and reused.

Mass Vaccination was very succesful!!
This is due to:
* High percentage of poppulation immunised.
→Low cost needed for mass production of vaccine.
→Many volunteers became vaccinators.
→Result in herd immunity.
* Infected people were easy to identify
→Few symtomless carriers.
→Can perform contact tracing and ring vaccination
→Can isolate cases to prevent spread.

Question 45

Why isn’t measles eradicated already

Answer 45

• MMR vaccine is available
• It is not eradicated even though there is a high coverage of vaccination.

Why
* Some children need several boosters
* Measles is highly infectious
→High percentage cover (93-95%) needed to acheive herd immunity.
→Must vaccinate whole population and infants less than 8months old.
* Diffucult for surveillance/to ensure vaccination.
→Due to high birth rates and high migration rates.
→Diffucult to give boosters, follow up on cases and trace contacts.

Question 46

Why isnt TB eradicated already?

Answer 46

BCG vaccine is available!
It is not eradicated even though there is a high coverage of vaccination!

Why?
* Vaccination does not work on adults older than 35 years old
* High percentage cover (above 90%) needed to acheive herd immunity.
→Not yet done in every country.

• Diffucult for surveillance/to ensure vaccination.
  →Due to high birth rates and high migration rates.
  →Latent TB is symptomless and found in 1 in 4 people.

Question 47

Why cant we vaccinate against malaria

Answer 47

• Proctoctists are eukrayotes.
  →Many more genes than bacteria and viruses.
• Display different antigens on its cell surface for;
  →Different species/strains
  →different stages of its life cycle
• Parasite changes antigens during infection.
  →Different genes coding for antigens during infection
• Plasmodium parasite hides in liver and RBCs.

Question 48

why cant we vaccinate against cholera?

Answer 48

• No effective vaccines against cholera.
• Oral vaccination only gives limited protection as it is excreted out of body.
  WHY
• many different strains against cholera
  →Bacteium mutates
• Vibrio cholera lives in the host intestines.
  →beyond reach of antibodies (antibodies are in blood stream).

Question 49

what is monoclonal antibody

Answer 49

Monoclonal=only one type of antibodt, specifif for 1 antigen.

Question 50

What is the problem when manufacturing antibodies in the lab

Answer 50

Isolated B cells that divide by mitosis DO NOT produce antibodies.
Plasma cells that secrete antibodies DO NOT divide.

Solution
Fuse plasma cells + cancer/myeloma cells
→hybridoma cells that CAN devide and CAN produce antibodies.

Question 51

How can we prouce monoclonal antibodies?

Answer 51

1) Inject foreign antigen (e.g. pathogen) into mice.
2) Allow time for immune response to occur.
3) Collect plasma cells from spleen
4) Fuse plasma cells with cancer cells to produce hybridoma cells.
→use fusogen for fusion
5) Clone hybridoma cells
→use HAT medium for hybridoma growth.
6) Screen for cells secreting desired antibody.
→by seperating cells and culture in induvidual wells.
7) Grow hybridoma cells in large scale culture.

Question 52

What is the usage of monoclonal antibodies?

Answer 52

1) Diagnosis
* Monoclonal antibodies have same specificity and detects only one antigen.
→Can distinguish between different pathogens/strains.
→Fast diagnosis than having to culture pathogen.
→Less labour intensive.
→Quicker diagnosis=quicker treatment

• Can be tagged with a fluoroscent label/dye
  →Can detect location of tissues expressing antigen.
  →Can detect location of tissues expressing antigens
  →For e.g cancer cells, blood clots
• Cheap, safe, fast results, easy to use and accurate.

2) Treatment
* Used to target specific diseased cell by binding to receptors on its cell surface.
→Can kill cell by stimulating the immune system.
→can attach radioactive substance/drug to Mabs to kill cell.

• Can bind to antigens on pathogens.
  →Result in artificial passive immunity.

Question 53

What are the problems of using Mabs in treatment.

Answer 53

• Causes some side effects
• Antibodies made in animals recognised as non-self.
• Trigger immune response in humans
  →Allergic reaction
• Remains in the body for short period of time as it is destroyed.
• Need to be administered more than once in small amounts.

Question 54

What is the solution to the problems of using Mabs in treatment

Answer 54

Humanise Mabs
1) Alter genes that codes for heavy and light chains of antibodies.
→Code for human antibodies instead of mice and rabbits.
2) Changing type and position of sugar groups attached to heavy chains.
→Arrangement of sugar groups same as antibodies.