2.4 cell recognition and the immune system

two flashacrds to add at the end abut how to answer certain questions, see notes

antigen

foreign molecule/protein/glycoprotein/glycolipid

that stimulates an immune response leading to production of antibody

how are cells identified by the immune system

each type of cell has specific molecules on its surface

often proteins have a tertiary structure

what type of cells and molecules can the immune system identify (4)

1. pathogens

2. cells from other organisms of the same species

3. abnormal body cells e.g. tumour cells

4. toxins released by some bacteria

describe phagocytosis of pathogens (non-specific immune response)

1. phagocyte attracted by chemicals / recognises antigens on pathogen

2. phagocyte engulfs pathogen by surrounding it with its cell membrane

3. pathogen contained in vesicle / phagosome in cytoplasm of phagocyte

4. lysosome fuses with phagosome and releases lysozymes (hydrolytic enzymes)

5. lysozymes hydrolyse/digest pathogen

where are antigens displayed

phagocytosis leads to presentation of antigens where antigens are displayed on the phagocyte cell surface membrane

stimulating the specific immune response

describe response of T lymphocytes to a foreign antigen ( the cellular response)

T lymphocytes recognise antigen presenting cells

specific helper T cells with complementary receptors bind to antigen on antigen presenting cell - activated and divide by mitosis to form clone which stimulate

• cytotoxic T cells - kill infected cells / tumour cells

• specific B cells (humorous response)

• phagocytes - engulf pathogens by phagocytosis

describe the response of B lymphocytes to a foreign antigen (the humoral response)

1. colonial selection

   specific B lymphocyte with complementary receptor binds to antigen

   this is then stimulated by helper T cells

   so divides by mitosis to form clones

2. some differentiate into B plasma cells - secrete large amount of antibody

3. some differentiate into B memory cells - remain in blood for secondary immune response

antibodies

quaternary structure proteins

secreted by B lymphocytes

bind specifically to antigens forming antigen - antibody complexes

structure of antibody

explain how antibodies lead to the destruction of pathogens

antibodies bind to antigen on pathogens forming an antigen-antibody complex

specific tertiary structure so binding site/ variable region binds to complementary antigen

each antibody binds to 2 pathogens at a time causing agglutination of pathogens

antibodies attract phagocytes

phagocytes bind to antibodies and phagocytose many pathogens at once

primary immune response

first exposure to antigen

antibodies produced slowly and at a lower concentration

takes time for specific B plasma cells to be stimulated to produce specific antibodies

memory cells produced

secondary immune response

second exposure to antigen

antibodies produced faster and at a higher concentration

B memory cells rapidly undergo mitosis to produces many plasma cells which produce specific antibodies

vaccine

injection of antigens from attenuated (dead or weakened) pathogens

stimulating formation of memory cells

explain how vaccines provide protection to individuals against disease

1. specific B lymphocyte with complementary receptor binds to antigen

2. specific T helper cell binds to antigen presenting cell and stimulates B cell

3. B lymphocyte divides by mitosis to form clones

4. some differentiate into B plasma cells which release antibodies

5. some differentiate into B memory cells

6. on secondary exposure to antigen, B memory cells rapidly divide by mitosis to produce B plasma cells

7. these release antibodies faster and at a higher concentration

explain how vaccines provide protections for populations against disease

herd immunity - large proportion of population vaccinated reducing spread of pathogen

large proportion of population immune so do not become ill from infection

fewer infected people to pass pathogen on / unvaccinated people less likely to come in contact with someone with disease

active immunity

initial exposure to antigen

memory cells involved

antibody produced and secreted by B plasma cells

slow - takes longer to develop

long term immunity as antibody can be produced in response to a specific antigen again

passive immunity

no exposure to antigen antibodies produced

no memory cells produces

antibody introduced from another organism

faster acting

short term

effect of antigen variability on disease and disease presentation

antigens pathogens change shape/tertiary structure due to gene mutations

no longer immune

B memory cell receptors cannot bind to / recognise changed antigen on secondary exposure

specific antibodies not complementary / cannot bind to changed antigen

e.g. yearly flu vaccines

structure of HIV particle

replication of HIV in helper T cells

1. HIV attachment proteins attach to receptors on helper T cell

2. lipid envelope fuses with cell surface membrane releasing capsid into cell

3. capsid uncoats, releasing RNA and reverse transcriptase

4. reverse transcriptase converts RNA to DNA

5. viral DNA inserted into helper T cell DNA

6. viral protein/capsid/enzymes are produced

   • DNA transcribed into new HIV mRNA

   • HIV mRNA translated into new HIV proteins

7. virus particles assembled and released from cells

explain how HIV causes the symptoms of AIDS

HIV infects and kills helper T cells as it multiplies rapidly

• so helpers T cells can’t stimulate cytotoxic T cells, B cells and phagocytes

• so B plasma cells can’t release as many antibodies for agglutination & destruction of pathogens

immune system deteriorates - more susceptible to infections

pathogens reproduce, release toxins and damage cells

explain why antibiotics are ineffective against viruses

viruses do not have structures that antibiotics inhibit:

• viruses don’t not have metabolic processes / ribosomes

• viruses do not have bacterial enzymes / murein cell wall

monoclonal antibody

antibodies produced from genetically identical / cloned B lymphocytes / plasma cells

so have same tertiary structure

explain how monoclonal antibodies are used in medical diagnosis

monoclonal antibody has a specific tertiary structure/binding site/variable region

complementary to specific receptor / protein / antigen associated with diagnosis

dye / stain / fluorescent marker attached to antibody

antibody binds to receptor / protein / antigen forming antigen-antibody complex

direct ELISA test to detect antigens

1. attach sample with potential antigens to well

2. add complementary monoclonal antibodies with enzymes attached - bind to antigens if present

3. wash well - remove unbound antibodies

4. add substrate - enzymes created products that cause a colour change

sandwich ELISA

1. attach specific monoclonal antibodies to well

2. add sample with potential antigens, then wash well

3. add complementary monoclonal antibodies with enzymes attached - bind to antigens if present

4. wash well - remove unbound antibodies (prevents false positive)

5. add substrate - enzymes create products that cause a colour change

use of antibodies in the ELISA test to detect antibodies

indirect ELISA

1. attach specific antigens to well

2. add sample with potential antibodies, wash well

3. add complementary monoclonal antibodies with enzymes attached - bind to antibodies if present

4. wash well - remove unbound antibodies

5. add substrate - enzymes create products that cause a colour change

what does ELISA stand for

enzyme-linked immunosorbent assay

what is the purpose of a control well in the ELISA test

compare to test to show only enzyme causes a colour change

compare to test to show all unbound antibodies have been washed away

discuss ethical issues with the use of vaccines and monoclonal antibodies

pre clinical testing on animals - potential harm, but animals not killed and helps produce new drugs to reduce human suffering

clinical trials on humans - potential side effects

vaccines - may continue high risk activities and pass on pathogen

use of drug - potentially dangerous side effects