Immonology 1 W1

Question 1

What is adaptive immunity?

Answer 1

Function is antigen recognition
- Young
- needs time
- is acquired
- lymphocytes
- Has memory
- different from person to person
- is specific pathogens

Question 2

What is innate immunity?

Answer 2

• Born with
• Doesn’t change
• Everyone has it
• Reacts exactly the same regardless of pathogens
• doesn’t learn
• non-specific

Question 3

Responsible cells the adaptive immune system

Answer 3

Lymphocytes, natural killer cells, macrophage, neutrophil, mast cell

Question 4

Responsible cells for the innate immune system

Answer 4

Phagocytic cells, epithelial cells, endothelial cells, natural killer cells, innate lymphoid cells, platelets

Question 5

What is the compliment system?

Answer 5

It has three pathways to activate and has three outcomes

Question 6

What is the lectin pathway?

Answer 6

Involves a bacterium

1- MASP-2 Cleves C4 into C4b and attatches to cell surface and C2 binds to C4b

2- MASP-2 cleaves C2 which is bound to C4b so we are left with C4b and C2b bound to form C3 convertase

Question 7

What is the classical pathway?

Answer 7

We start with an antigen at tea body complex

1- CLs cleaves C4 into C4b and attached to the cell surace. C2 binds C4b

2- CLs cleaves C2 to C4b to get C4b and C2b to form C3 convertase

Question 8

What is the alternative pathway?

Answer 8

We start with a microbial surface with C3b already attached from the amplification loop

1- B binds to bound C3b

2- D cleaves B bund to C3b to give C3 convertase

Question 9

What do all the pathways end with

Answer 9

They all form C3 convertase

C3 is cleaved to form C3a and C3b which go onto have effector actions

C3b goes back into amplification loop for the alternative pathway as it is good at binding to bacteria

Question 10

What are the three outcomes

Answer 10

• Inflammatory peptide
• Form C3b for alternate pathway
• Form C5b hind bid to 6,7,8,9 to form MAC

Question 11

C3a and C3b

Answer 11

C3a - inflammatory peptide
C3b - attach to surface and make bacteria more visible to phagocyte

Question 12

C3

Answer 12

are enzymes but not active in blood stream. Only formed with a reason ie an infection. Can only do something when they are cleaved or bound to another to eventually form the converatse enzyme. We just need to activate these protein and so it is fast as we dont have to wait for the proteins to be made.

Question 13

NK cells

Answer 13

Crucial in killing cells that aren’t working properly too not just infections

2 functions:
• killing infected cells
• Help other cells - release natural cytokines

Float and try to interact with as many cells as possible

Question 14

MHC 1

Answer 14

Major histocompatible class

On everybody cell that has a nucleus

Most common cell marker an NK cell recognises as “self”

MHC-1 on target cell attaches to NK cells inhibitory receptor and turns the killing function off so NK moves to another cell

Question 15

So how do natural killer cells activate and deactivate?

Answer 15

An NK cell has an activator receptor and an inhibitory receptor on its cell surface

A healthy cell or have an activator ligand and an MHC-1

When all four of these binds together, there is no death as the inhibitory receptor is activated

A virus infected cell does not have MHC -1 on its surface and so cannot bind to the inhibitory receptor. The activator Ligand and activator receptor bind and so the virus infected cell is killed.

Question 16

Five ways of cell death

Answer 16

1. Perforin
2. Granzyme
3. FasL
4. TNF-d
5. IFN-y

Question 17

What is the IFN system?

Answer 17

It is important for protection against viral infections

1. There is a cell with a virus attached.
2. The cell produces IFN-a and IFN-b
3. This activates and attract natural killer cells.
4. The IFN-a and IFN-b signal to surrounding cells that there is a virus and to protect themselves from infection

Question 18

Signal transaction of IFN

Answer 18

1. The IFN vines two receptors and the two receptors come together
   2.JAK is phosphorated and activated
2. Two receptors come together to form a dimer.
3. The transcription factor STAT is activated.
4. The STAT and JAK bound to the two receptors and IFN
5. Proteins are produced from binding to elements of DNA in nucleus.

Question 19

Stages of inflammation

Answer 19

1. We get infected by bacteria and compliment activation of mask cells to release histamine.
2. This causes vasodilation where the vessels widen to let more blood flow through, but also makes them leaky which leads to swelling.
3. There is mitigation migration of neutrophils whereas sites force themselves between the end of the themselves of the blood vessel and migrate into the tissue.
4. Phagocytes are attracted via chemokines and chemotaxis.
5. Phagocytes destroying microorganisms and any changed/mutated or dead cells.
6. Damaged Tissue is repaired.

Question 20

Prostaglandins

Answer 20

1. There is a stimulus from an injury.
2. There is activation of phospholipid A2
3. This turns phospholipids into Arachidonicacid
4. Lipooxygenases transforms this into 12-HETE, 15-HETE, LT4 or can be made into PGH2 prostaglandins by cyclooxygenase COX-1 and COX-2

Question 21

What is cyclo-oxygenase blocked by?

Answer 21

NSAIDs block COX-1,2
• blocks production of prostaglandins
• We dont want to block COX-1as is always active in body for GI function etc
• COX-2 only activated when have inflammation response
• Ideally only want to block COX-2 to prevent side effects of fever etc
• We have no drugs selective to COX-2

Question 22

So the immune system all at once

Answer 22

all at the same time

1. We have tissue damage and get bacteria infection
2. Compliment activation produces C3a ad C5a which leads t production of mast cells which release histamine, prostaglandins and leukoteirns
3. Get weak endothelial layer and cells are attracted in to tissue
4. Monocyte is immature macrophage
5. Monocytes in the blood and become macrophages in tissue
6. Compliment activation also gives C5b and C7
7. C3b bind to bacteria and allow macrophages to come and eat them
8. C5a attracts neutrophils too = chemotaxis
9. Macrophages release chemokines and lekotriens etc when activated which draws in more neutrophils

Question 23

How many antibodies do we have?

Answer 23

10 to the power of 80

Question 24

Non-clonal

Answer 24

Every cell that is divided (daughter) has the same receptors as the original cell

Question 25

Clonal

Answer 25

Every time B cells are dividing they change overtime and her daughter sells produce a slightly different antibody

Question 26

MHC class 1

Answer 26

Protein on the cell surface of every nuclear cell in the body

Works with cytotoxic cells

Question 27

MHC class 2

Answer 27

Found on antigen presenting cells (macrophage),B cells and dendritic cells which will also have class one
Work with Helper T cells

Question 28

Pathways of intracellular processing of protein antigens (2 pathways )

Answer 28

Helper
- Recognise his antigens on surface of MHC2
-Engulfs the pathogen and processes it into smaller peptides
-Peptides all loaded onto MHC2 within the APC
-MHc2 peptide complex is transported to the cell surface

Cytotoxic
- Recognise antigens on the surface of MHC1
-Get infected
- Processes antigens into smaller peptides
-Loaded onto MHC1
-Transported to the surface

Question 29

T cell development

Answer 29

Made in bone marrow and migrate thymus to mature
Begin as CD4- and CD8- (too young)
TCR -b recombination forms CD4+ and CD8+
They need a receptor to be able to be activated, do they want to be helper or cytotoxic
TCR -a recombination goes through positive and negative selection but cannot leave the thymus yet as not H or T
Help cells are CD4+ and CD8-
Cytotoxic cells are CD4- and CD8+

Question 30

Positive and negative selection of T cells in the thymus

Answer 30

When there is no selection there is no binding and so there is apoptosis as the receptor won’t recognise the T complex

Positive Selection is the best as there is weak binding and the T cell bind with the peptide

Negative selection is strong binding and strong is not good as the complex could become activated by an MHC without an infection or antigen and activated cytotoxic could cause tissue damage.

We only want them activated when they needed.