Defence Against disease 2 Flashcards
How do B lymphocytes defend the body ( vague)
Create humeral immunity
Dispatches antibodies in the bodies humours, fluids, blood and lymph
Stages of B lymphocytes defending an attack
1) identify antigen from pathogen : bacterium, fungus, toxin or virus
2) pathogens bumps into complimentary B cell, the one with the correct antibodies and binds to it (clonal selection)
3) B cell is then activated by t helper causing the b cell to proliferate clone rapidly, forming many cells with the exact same antibodies.
4) effector cells mass produce antibodies (2k per sec) for 4/5 days
5) antigens move round the body binding to as many antigens as they can, neutralisation or agglutination stops damage until pathogens engulf
humoral immunity
B lymphocytes maturing process
Mature fully in the bone marrow
Once mature they have unique antibodies on the membrane of each cell, up to 10k
Helper T cells help mature naive effector B cells by binding to them and releasing cytokines
How do t lymphocytes defend the body ( vague)
Cellular immune response
Cause immflamuation, activate macrophages, regulate immune response, fire up other T cells
Stages of how T cells defend the body, cell mediated immunity
1) in the non specific defence system macrophages engulf and digest pathogens and display their antigens on their cell surface (APC’s )
2) receptors on some of the 2 cells fit these antigens, they bind and release interleukin stimulating more 2 cells to divide by mitosis. they form clones of the activated t helper cell that all carry the right antigen to bind to a particular pathogen
3) cloned t cells may: differentiate into t memory cells, produce interleukins that stimulate phagocytosis produce interleukins that cause b cells to divide, stimulate the development of a clone of T killer cells that are specific for the presented antigen
What are professional antigen presenting cells
Macrophages that engulf pathogens and display pathogens antigens on their cell surface
What to regulatory T cells do
Release anti cytokines
Clonal selection
Correct\complimentary helper T cell binds to antigen presenting cell
Interleukin is released
Clonal expansion
Interleukin produced by helper T cells after binding to correct APC
This activates the B cells
Stimulates T cell replication, memory, killer, helper
The activated B cells divide by mitosis to give clones of plasma cells and b memory cells
Simple immune response
Nature of Antigen encountered, colonial selection , colonial expansion, differentiation, action
T helper cells
Bind to the surface antigens on APC’s
Produce interlinking , which as a type of cytokines
Interleukins
Stimulate the acuity of B cells, which increases antibody production , stimulates production or other types of T cells, and attracts and stimulates macrophages to enter the area
General Antibodies structure
Large proteins known as immunoglobulins
Specific shape that is complementary to a specific antigen
4 polypeptide chains held together with disulphides bridges
2 long identical chains called heavy chains
2 shorter identical chains called light chains
Antibody structure relating to function
Variable region - area of specificity, to an antigen, due to amino acid sequence. Located at the top of the Y
Hinge region- found between the long chains and short chains, allows flexibility for attachment to more than 1 antigen. Joining point of the Y
Constant region- same on all antigens ( main part of the Y) allows attachment to phagocytes
Ways in which antibodies defend the body
Antibody of antibody-antigen complex acts as an opison so complex is easily engulfed
Pathogens are neutralised, so they can no longer invade host cell
Antibodies act as agglutinins causing pathogens carrying antibody-antigen complexes clumped together
Antibodies can act as antitoxins
Active immunity
Already exposed to the pathogen, so body already has memory cells.
Antibody production is quick
Vaccination = artificial active
Passive immunity
Artificial passive - injection of antibodies
Natural passive, mother giving baby chloesterin full of antibodies
Offers protection for a month
Autoimmune diseases
Disease where the immune system mistakenly identifies your own cells as “foreign” rather than “self”
There are no cures: treatments are, immunosuppressants that slow down the immune system
What factors increase the risk of autoimmune diseases
Genetics
Obesity
Sex - women
Types of autoimmune diseases
Diabetes type 1 - destruction of pancreatic cells
Rheumatoid arthritis- damage to joints
Lupus - inflammation to lining of organs
What vaccines contain
Killed or inactivated bacteria and viruses
Attenuated (weakened) strains of live bacteria or viruses
Toxin molecules that have been altered or detoxified
Isolated antigens extracted from the pathogen
Genetically engineered antigens
Process of vaccination
Small amounts of save antigen, known as the vaccine, are injected into the blood
Primary immune response is triggered by foreign antigens, body produces antibodies and memory cells as if you were infected with the live pathogen
If you come into contact with the real pathogen the secondary immune response is triggered
How vaccination changes due to pandemics or epidemics
Mass vaccination to to the spread
Herd immunity once enough of the population is vaccinated
Sources of medicine
Penicillin- mould and fungus (melons) Docetaxel - yew trees Aspirin - willow bark Prialt- snake venom Vancomycin- soil fungus Digoxin- fox gloves
Synthetic biology
Use of genetic engineering
Uses bacteria as a biological factory
Populations of bacteria are modified to produce much needed drugs in larger quantities than we would ordinarily have access to
Development of antibiotic resistance
Random mutation occurs that makes some bacteria slightly more resistant, bacteria pass this mutation on to daughter cells
Farmers in the US routinely adding antibiotics to animal feed.
this accelerates natural selection.
Over prescription/ not fishing prescribed course of antibiotics leads to antibiotic resistance
Means some antibiotics may become useless
Use of antibiotics in 20th century
Large number of death were due to communicable diseases
Antibiotics interfere with the metabolism of bacteria without affecting human cells - selective toxicity
How do cytokines stimulate B lymphocytes
Cytokines has specific shape, complemnartyu to receptor
Cytokines binds to receptor on cell surface membrane
This activates clonal expansion
How does HIV take over the host cell
Viral DNA inserted into host nucleus
Viral RNA and mRNA transcribed
To code for viral proteins
Humoral immunity
Body responds to antigens found outside cells e.g free floating pathogens
Purpose of the constant reigon
Allows binding to phagocytes
Speed of production
Role of memory cells
Memory cells recognise display complimentary antigens to the pathgoen, binding to it (clonal selection)
Memory cells undergo clonal expansion dividing by mitosis to produce clones which then differentiate into plasma cells that produce antibodies
Help destroy viruses before symptoms appear
How HIV takes over host cell
Revrse transcriptase inserted into host nucleus which converts the RNA which has also been inserted to DNA
The viral DNA is transcribed to produce viral RNA which is then translated to produce viral proteins
how phagocytes are able to pass into the tissue fluid
they have a : narrow nucleus, a flexible cell structure
histamines make capillary walls leaky allowing phagocytes to squeeze through more easily
