Lecture 7- Antibodies in Infection Flashcards Preview

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Flashcards in Lecture 7- Antibodies in Infection Deck (23):
1

How do antigens get to secondary lymphoid organs

1) blood/lymphatic fluid, uptaken by dendritic cells that transport

2

Describe how foreign antigens meet the IS, through things like the skin or GI tract

Foreign antigens enter our system, and are meet by dendritic cells (eg- langerhans cells).
The dendritic ingest and process this material, then travels through the lymph to lymphnodes, and present this material via APC.
Here they interact with B and T cells specific to the antigen

3

What are the two classes of lymphocytes

Effectors : AB production (B cells, elclusively effectors), NK cells, CD8 T lymphocytes.

Regulators: Cytokine production CD4 T lymphocytes, helper T cells, regulatory T cells

NOTE T-cells are both effectors (CD8) and regulators (CD4)

4

How are shapes recognised

1) recognise common characteristic of many substances (non-specific immunity)
2) recognise uncommon characteristic of a particular foreign substance. (specific immunity)
3) recognise common things in uncommon context

5

Difference with what B and T cells can recognise

B lymphocytes = wide range of antigens
T lymphocytes = short peptide antigens

6

antibodies/immunoglobins (Ig) look like? Draw and label

...

7

How are antigen specific lymphocytes activated

Antigen binds > change in surface cell receptors > antigen-specific signal > alerts the cell > cell decides whether it will respond or not

8

If Bcells or T cells respond, what happens?

B cells > production of that same antigen specific AB

T cells > either CD8 or CD4 production

9

Epitope

specific part of antigen that binds to the AB

10

Primary response

When an animal responds to an antigen it has never previously met.
Lag of a few days (no AB able to recognise) before specific AB appear in the blood (virgin B cells will recognise and start to pump out specific AB), that can bind to the specific antigen and lead to its neutralization/ removal.

11

Secondary response

animal exposed to same antigen later in life, response is much more rapid and vigorous and for much longer. IS has memory B cells of this antigen, and a build up of AB

12

How do B cells generate AB response?

Antigens bind to surface Ig receptors on Bcells in secondary lymphoid organs. If bound with a high enough affinity they overcome activation threshold. (also extra activation by Helper T cells).
Activation of these B cells results in proliferation of
-population of memory identical to the precursor B cell that can be restimulated for a secondary response
-population of plasma cells which secretes the same antigen specific ABs.

13

Why does it take a long time for an antigen to bind to a antigen specific Bcell

Because although they have 1000s of receptors they are only specific to one shape, takes a long time to find a match!

14

Memory B cells

- replace original B cells
- respond to a much lower conc
-live longer
-there are many more

for the SECONDARY response

15

Explain the difference of our ABs in utero to post birth

In utero: all AB from mum, build up
Post birth: mums decline, we start to make our own, this is a vunerable period.

16

Four ways which ABs work

1- Direct Neutralization
2- Opsonisation
3- AB-dependent cell-mediated cytotoxicity
4- Complement activation

17

Direct neutralisation

Coats things, physical stops the potential harm getting to where it wants to infect

18

Opsonisation

"enhanced phagocytosis"
AB coat foreign material, and now phagocytic cells can bind with a higher affinity , increasing the effectivness of phagocytosis.

This is because the Fc region of the antibody has a high affinty for neutrophils (Fc receptors on phagocytic cells)

19

Antibody-dependent cell mediated cytotoxicity

K cells (small pop. of lymphocytes) have Fc (AB) and C3b (complement) receptors and can kill this cellular material short range cytotoxicity.
(They are NOT phagocytic)

20

Complement activation

Series of 20 proteins in blood that act as an enzyme cascade, that amplifies small signals.
Antigen-AB complexes can trigger the 'classical pathway' of this.
Results in Chemotaxis, leakage, and membrane lysis that all help to destroy/remove foreign material.

21

What of the the complement system binds to antibodies and where

Early components at CH2 on AB

22

How is the opsonisation and membrane lysis linked

Opsonisation provides focus fro the later complement system, that attach themselves to C3 and forma biochemical donut that inserts itself into the membrane next to C3b = cell lysis.

23

Draw the classical and alternative pathway of the complement system.

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