Adaptive Immune System

what is the adaptive immune system

• is specific, can recognise and react to different pathogens with different responses due to different receptors coded for in our genes

• has a great diversity of possible responses to pathogens

• has memory

• capable of self-tolerance (doesn’t attack itself)

what is the humoral response?

• effective against pathogens in body fluids

• utilises B cells

• characterised by the production of antibodies

what is the cellular response?

• effective against intracellular pathogens (pathogens inside host cell)

• utilises T cells

• characterised by the destruction of infected cells

how are antigens recognised?

• T and B cells have specific receptors which can bind to antigens on their cell surface

• Each T and B cells has a unique antigen receptor which can bind to one type of antigen

• different receptors coded for in the genes are present from birth

what is the cell mediated response?

• T cells target and destroy infected cells

• T cells can bind to infected cells via the receptors on their surface

• this cell mediated immunity is effective in defending the body against:

  • pathogens inside cell

  • macroparasites

  • tumour cells and transplanted tissue

• antibodies cant get to pathogen inside cell therefore cell-mediated response is needed

  • uses chemicals for the attack of the infected cell

what do the T cells and MHC molecules do?

• T cells recognise fragments of antigens which are displayed on the surface of the cells

• allows T cells to recognise antigens that have been partially digested by macrophages, etc

• specific surface markers called MHC molecules are involved in recognising self-cells

  • bind to peptide fragments of digested antigens and display them on the cell surface for recognition by T cells

what does MHC I do?

• cell infected pathogen will display fragments of the pathogen on its MHC molecule

what does MHC II do?

• antigen presenting cells, activated B cells and macrophages, present the antigen fragments on MHC II molecules.

what are T lymphocytes

• produced in bone marrow

• mature in thymus gland

• released into blood and migrate to lymph nodes and other parts of the body

how all the cells work together?

1) antigen presenting cells (B cells, macrophages, dendritic cells) migrate to the lymph nodes

2) receptors on the surface of a specific T helper cell bind to the antigen

3) activates the T helper cell and stimulates the release of cytokines

4) cytokines have a variety of effects, including stimulating T cells to rapidly clone and produce cytoxic T cells that bind to infected cells and kill them through the release of more cytokines

5) cytokines cause infected cell to die by triggering lysis by apoptosis

6) cytokines also attract phagocytes (chemokines) to the area to clear up the cell debris and trigger inflammation (histamine and prostaglandin)

7) when the production of cytoxic T cells is triggered, supressor T cells and memory T cells are also produced

how are b lymphocytes made?

• responsible for adaptive immune response outside cells

• made in bone marrow,

• stored in lymph nodes,

• circulate in the blood

how are B lymphocytes activated and what do they do?

• activated by cytokines released by Helper T cells

• activated by binding to an antigen

once activated:

• make copies of themselves (clone)

• differentiate into 2 possible cell types:

  • plasma cells - they are capable of making antibodies

  • memory B cells - remember the pathogen for subsequent infection

what are antibodies?

• molecules produced by plasma cells in response to a certain pathogen

• also called immunoglobulins

• act to neutralise a pathogen

ways antibodies neutralise a pathogen? 3

• antigen neutralisation

  • bound antibodies block antigens from binding to other targets, prevent toxins from destroying a cell

• agglutination

  • pathogen becomes trapped in a network of antibodies, making them immobile + susceptible to destruction.

  • remember glued together

• complement activation

  • bound antibodies activate a cascade of compliment proteins

  • complement protein can punch holes in the pathogen or create an inflammatory response which attracts macrophages and neutrophils.

flowchart of the process 🙈

how do T and B cells interact?

• they both attack the anitgen

• Helper T cells assist in interaction by releasing chemicals (cytokines) to stimulate B cells and T cells to clone

• B cells can also activate Helper T cells

• if a B cell encounters an antigen it binds to the antigen and presents it to the helper T cell

• T helper cells release cytokines that activate more Helper T cells and macrophages

outline the third line of defence?

• vaccine enters and triggers inflammatory response

• initially mediated by the non-specific immune system

• dendritic cells are attracted to antigen

  • antigens are taken up by dendritic cells and presented on the cell surface membrane; migrate to lymph nodes

• T cells that recognise specific pathogen being presented by dendritic cell bind to the anitgen

  • process activates T cell to become helper T cell

• immature B cell pick up antigen on there surface by immunoglobulins

  • helper t cells bind to antigen on the B cell then releases cytokines that stimulate the B cell

• once stimulated, B cell go through rapid proliferation, differentiating into plasma cells and memory B cells

• further stimulation of B cells by T cell action leads to affinity maturation where the affinity antibodies are produced

• when infection is over, plasma cells die off, antibody concentration falls

  • contraction phase

second response of encountering the same disease?

• adaptive immune system retains memory of the anitgen for future use

• continue to secrete low level of high-affinity

  • immunological memory

• when body exposed to same antigen the high-affinity antibodies in the blood bind to the antigen

  • acts as a signal

• memory B cells and T cells are activated faster

• memory B cells proliferate into plasma cells in higher concentrations

• there further muturation, cells are more specific

• antibody becomes quicker, more sustained, higher-affinity

what happens to T and B cells when the T helper cell with complementary antigen receptors activated?

why is the primary immune response slower?

• the time taken to fight an infection is longer because once antigen has been identified appropriate T cell and B cells have to be activated.

  • takes time to build clones of these cells

  • called the lag phase 4-7 days (can be longer)

• time needed for the cytotoxic T cell to kill infected cells + for the B cells to produce plasma cells that secrete antibodies that bind with the antigen to neutralise it

  • antibody peak is 7-10 days after infection

• if sufficient antibodies are made to destroy all infecting antigens, person recovers completely:

• primary immune response

• same time memory T cells + memory B cells specific to antigen are produced and remain in the body

why is the secondary immune response faster?

• if same antigen reentered the body, the second response if quicker

• after identification of antigen, memory cells activate the production of the cytotoxic T cells + B cells

• large number of B cells from many plasma cells, secrete larger amounts of antibodies than in primary response

  • lag phase reduced to 1-4 days

  • antibody peak is 3-5 days after infection

• effect is to destroy invading antigens before their numbers are large enough to cause symptoms

• secondary response is:

  • quicker

  • requires less antigen to intiaite it

  • produces a much greater quantity of antibodies

Comparing immune responses

Feature	Primary Response	Secondary Response
Definition	The reaction of the immune system when it contacts an antigen for the first time	The reaction of the immune system when it contacts an antigen for the second time and subsequent times
Responding Cells	Naive T + B cells	Memory T + B cells
Lag Phase	Long (4-7 days)	Short (1-4 days)
Antibody Peak	Antibody level reaches peak in 7-10 days	Antibody level reaches peak in 3-5days
Strength Of Response	Weaker than secondary	stronger
Antibody Level Over Time	Declines to the point where it may be undetectable	Tends to remain high for longer

graph of primary and secondary response explain every number

1) antigen is detected by immune system, B cells activated

• divide to produce plasma cells, that produce antibodies

• takes time, causing lag phase 4-7 days

• memory B cells also produced

2) as more plasma cells are produced, amount of antibody released increases

3) antibody peaks

• pathogen destroyed

• antibody production decreases as less anitgen present

• memory cells are still present

4) memory T cells activate memory B cells which quickly differentiate into plasma cells, produces large amounts of antibody quickly

• high peak of antibody due to presence of more plasma cells producing antibodies

• pathogen destroyed before symptoms begin

5) antibody production decreases as fewer antigens present

• more memory T + B cells have been formed

what is inside the vaccines - three types?

• vaccines contain cultures of microorganisms, may either be:

  • living but attenuated - weakened - therefore harmless, rabies

  • dead, typhoid

  • contain toxins called toxoids (tetnus)

    • vaccines may be given orally or by scratching skin surface

  • may use nucleic acids, mRNA, DNA

how do vaccines work?

• are all harmless to the body, will ot cause the disease they are specific for

  • some contain antigens that make your body undergo an immune response + produce memory cells for that particular antigen

• if body is exposed to antigen in future, secondary response is activated

  • antigen destroyed before symptoms of disease are experienced

• immunity formed is lifelong to the one type of disease

compare vaccination to immunisation?

• vaccination involves introducing vaccine into body

• immunisation is a process where the body reacts to the vaccine by going through the immune response, producing memory cells for the antigen

  • confers immunity to the body so if antigen enter in future secondary response occurs - no symptoms suffered

what is the effectiveness of vaccines?

• a series of vaccines should be given over a number of years

  • each vaccine introduced produces small response

  • a series of vaccinations, lymphocytes will more rapidly recognise the antigen and the number of memory cells will be enough for a long time

  • # of memory cells can decrease over time, booster injections neededto increase number of circulating memory cells, ensures disease is maintained

    • e.g. booster injections given to maintain immunity for tetanus and whooping cough as the number of memory cells for this decreases over time.

what is passive acquired immunity?

• involves introducing antibodies (immunoglobulins) into the body to prevent a disease from developing

• these antibodies are produced by another organism that suffered the disease

• E.g. being exposed to disease Hepatitis A, you may be given injections of immunoglobins to preent you from contracting the disease

  • Immunity will last for only a couple of months no memory cells have been produced

what is herd immunity?

• form of indirect protection from disease that happens to individuals when most of population around them is immune

• vulnerable people who haven’t been exposed to or vaccinated against disease are safer and it cant spread easily

what is polio?

• virus transmitted by oral contact, with secretions or faecal material from infected person

• Most cause no symptoms with viral replication limited to cells of the digestive tract

• Less then 1% of infections, polio virus invades the nervous system and can cause irreversible paralysis

• People with paralysed respiratory muscles may spend the rest of their life in iron lungs

• There is no cure and no medication, but since 1955 there have been safe and effective polio vaccines