Immunology Flashcards
Describe how antibodies are produced in the body following a viral infection
- virus contains antigen;
- virus engulfed by phagocyte / macrophage;
- presents antigen to B-cell;
- memory cells / B-cell becomes activated;
- (divides to) form clones;
- by mitosis;
- plasma cells produce antibodies;
- antibodies specific to antigen;
- correct reference to T-cells / cytokines;
What is an antigen
Molecule usually a protein
That stimulates an immune response
Resulting in the production of a specific antibody
Pathogen
A disease carrying microorganism
How do pathogens cause disease and harm
Release toxins which can directly damage tissue
Replicate inside host and destroy it
What do antigens allow the immune system to identify
Pathogens Toxins Abnormal body cells Cells from other organisms of the same species Foreign cells
Phagocyte
Type of leukocyte
Capable of distinguishing between cells that do and don’t display the correct antigens
Detect chemical signals
Engulf and destroy foreign antigen presenting cells through phagocytosis
To become an antigen presenting cell
Phagocytosis
Pathogen engulfed by phagocytosis
Enters cytoplasm in a vesicle called a phagosome
Lysosomes fuse with the phagosome
Releasing hydrolysis digestive enzymes called lysozymes
Pathogen hydrolysed
Waste material removes via exocytosis
Phagocyte becomes an antigen presenting cell, displaying the pathogens antigen on its cell surface membranr
What is phagocytosis by definition
Part of non specific immunity
Where pathogen is engulfed, hydrolysed and destroyed by a phagocyte
Specific immunity
Specific response to a specific antigen on the surface of a cell or pathogen
That has been recognised as non self
What are the stages of cellular response
Antigen presenting
Clonal selection
T cells
Explain cellular response
Th cells can respond directly to pathogen or respond to an APC that presents the specifically complementary antigen
Phagocytosis means Th cells can bind to the presented antigen
Therefore activated
Then rapidly one by mitosis
In clonal selection
Role of helper T cells
Specific Th cell binds to APC and when activated rapidly divide by mitosis for clonal selection
Release cytokines that attract phagocytes to the area of infection
Release cytokines that activate cytotoxic killer T cells
Activate specifically complementary B cell
Form memory Th cells
Cytokines
Released by helper T cells
Attract phagocytes to the area of infection
Activate cytotoxic killer T cells
What is the role of cytotoxic killer T cells
Locate and destroy infected body cells that present the correct antigens
Bind to APC
Release perforin (protein) which creates holes in the cell surface membrane and causes the APC to be destroyed
Role of memory T cells
Remain in the blood long term
Can recognise foreign antigens to respond rapidly and extensively upon second infection
Why is clonal selection needed
Wouldn’t be enough room in the body to have lots of every T cell for every antigen you may ever encounter
Increased number of cells woukd increase the total energy demands of organism
Humoral response
A stage of primary response
That involves the activation of B cells to produce antibodies
B cells must be stimulated by their complementary Th cell
By the release of cytokines
Explain B cell activation
A specific Th cell with the correct receptor binds to presented antigen and locates and activates the specifically complementary B cell
Specific Th cell releases cytokine chemicals which signal the specific B cell to clone by mitosis (clonal selection)
B cell then differentiates into: plasma cells which produce and secrete vast quantities of the specific antibody into the blood
And memory B cells which remain in the body to respond rapidly and extensively if a future reinfection occurs for the same pathogen
Similarities between primary and secondary response
Both involve memory B cells
Both involve antibody production
Differences between primary and secondary response
P: first time in contact with the pathogen/S: reinfection
P: takes longer to establish immune response/S: rapid and extensive
P: response by naiive B cells and T cells/S: response by memory B cells
P: antibody peak reaches in 7-10 days/S: peak 3-5 days
P: antibody levels decline rapidly/S: remain high for longer time
Types of non specific defenses
Physical barriers: mucus, stomach acid, ear wax, blood clotting, lysozyme in tears
Phagocytosis: engulfs and destroys
Immediate response
Same for all pathogens
Types of specific defenses
Cell mediated: T lymphocytes
Humoral: B lymphocytes
Slower response
Specific to each pathogen
What is an antibody
A quaternary protein made in response to foreign antigens
Has a binding site specific to one antigen
Specific antibody produced by specific plasma cell
Structure of an antibody
Quaternary protein of 4 polypeptide chains
Y shape
Constant region that’s the same for all antibodies
Variable region has a different primary structure so different tertiary structure
Variable region where the specific binding site is
Can only form antigen antibody complex with the one
Epitope=specific region of antigen that antibody binds to
4 ways antibodies assist the destruction of a pathogen by preventing its replication
Agglutination
Opsonisation
Lysis
Anti toxins/venom
Agglutination
Specific antibodies bind to the antigens on the pathogen and clump them together
Opsonisation
Marking pathogens so phagocytes recognise and destroy the pathogen more efficiently
Lysis
Bind to antigen and lead to destruction of the pathogens membrane
Antitoxin/antivenom
Bind to toxin or venom (protein)
To prevent them binding to their specific complementary target receptors
How are B cells activated
Indirectly by specific Th cell with correct receptor that can bind to presented antigen, locate and activate B cell
Memory B cells not involved directly in destroying pathogen but on reinfection, rapidly activated by cytokines
Directly activated when B cell detects the antigen via antibodies
Explain the secondary response
Rapid and extensive
Antigen is usually eliminated before it can cause disease or any symptoms to develop
More antibodies produced more rapidly
Defined as the activation of memory cells to produce antibodies
Explain antigenic variation
Random mutations of pathogens antigens
Making it hard to develop vaccines since no longer recognisable to memory cells (no longer complementary to receptors)
Can’t initiate secondary response
Passive immunity
Type of immunity where no exposure to antigen
Antibodies recieved from elsewhere/not produced by individual
No memory cells produced
Short term and fast acting
Passive immunity examples
Antiserum
Placenta
Breast feeding and milk
Active immunity
Type of immunity where antibodies are produced in response to exposure to an antigen
Memory cells produced after a primary immune response
Long term but slower acting
From contracting an illness and fighting it off or a vaccine
Passive vs active immunity
P: No antigen exposure/A: Antigen exposure
P: Antibodies not produced by individual and recieved from elsewhere/A: Antibodies produced in response to antigen
P: No memory cells produced/A: Memory cells produced after primary immune response
P: Short term protection/A: long term
P: Antibodies eventually broken down/A: Memory B cells circulate in blood for years
P: Fast acting/A: Slower due to primary response
How does a vaccine work
Contains antigens from dead, weakened or attenuated pathogen
Pathogen engulfed by phagocytes and displayed on the antigen presenting cell
Specific T Helper cell binds to APC antigen
Stimulates a specific B cell by releasing cytokines
B cell divide by mitosis to produce plasma cells and memory cells in clonal selection
Plasma cells produce and release the complementary antibody
Memory cells recognise antigen on second infection
Not effective against pathogens showing antigenic variation
Purpose of boosters
Increase effectiveness of vaccinations
Acts as a memory cell top up so that on infection there are enough memory cells to divide into plasma cells to combat pathogen with antibodies
Outline vaccine ethics
Side effects vs benefits: usually mild causing fever but could be severe and permenant
Animal trials and animal rights
Human trials: who and how much risk
Affordable for everyone
Should we be eliminating an organism and loss of generic variation
Why don’t vaccines provide protection against antigenic variation
Vaccine contain specific antigen of attenuated pathogen
So only provide immunity against that pathogen
Antigens mutate and can change shape
No longer complementary to specific B cell/antibody
No secondary immune response
What is herd immunity
Enough individuals in a population are vaccinated
85%
So little chance of the disease spreading
Even non vaccinated individuals protected
What are monoclonal antibodies
Antibodies produced from a single group of genetically identical plasma cells
With a unique tertiary structure that binds to only one type of antigen
Uses of monoclonal antibodies
Research Immuno assays (pregnancy or elisa) Diagnosis Targeting drugs Killing specific cells Isolating specific chemicals
Ethics of monoclonal antibodies
Similar to vaccine ethics
Unethical to induce tumours in mice which are genetically engineered to produce human antibodies
A few cases of volunteers experiencing unexpected side effects
Antigenic drift
Small random mutations of pathogens antigens
Antigenic shift
New strain develops from mutation of pathogens antigens
True negative
Test says you don’t have it
You don’t have it
True positive
Test says you have it
You have it
False negative
Test says you don’t have it
You have it
False positive
Test says you have it
You don’t have it
Why do blood transfusions work sometimes but not long term
Blood contains memory cells and plasma cells which can produce and release specific antibodies
So transfers antibodies and acts as a form of passive immunity
Antibodies can then bind to the specific antigen on pathogen
Leading to the destruction of the pathogen in patient
Patients immune system will start to break down the plasma cells because seen as foreign
So won’t provide long term protection because antibodies are destroyed if plasma cells are destroyed
What is an ELISA test
Enzyme Linked Immunosorbent Assay
A method of measuring the amount of antigen or antibody in a sample
Involves monoclonal antibodies with attached enzyme that catalyses an easily detectable substances
Explain the process of an ELISA test
Test uses monoclonal antibodies to detect a certain substance in a sample of liquid
- Monoclonal antibodies fixed to surface of test well
- sample containing molecule to be detected/positive control binds to antibody due to complementary shapes
- Second monoclonal antibody with enzyme attached added and binds to molecule (conjugates)
- Washed to remove any excess unbound antibodies with enzyme to prevent false positive
- Substrate for enzyme added
- Chemical colour change visible means that the enzyme is present and hence antibody bound so positive result
How does a pregnancy test work
Detects HCG hormone (Human Chorionic Gondatropin) found in the urine of pregnant women
- Application area contains antibodies for HCG bound to a coloured blue bead
- Urine applied, any HCG in urine binds to antibody on the beads
- Forming an antigen-antibody complex
- Urine moves up the stick to the test strip, carrying any beads with it
- Test strip contains antibodies to HCG that are immobilised
Present: test strip turns blue since immobilised antibody binds to any HCG, concentrating the HCG-antibody complex with the blue bead attached
Not present: beads pass through test area without binding to anything so won’t go blue
Why can antibodies only bind to one type of antigen
Quaternary proteins with a specific 3D tertiary structure determined by the unique primary structure
As a result they have 2 unique binding sites complementary in shape to only one type of antigen
So only form an antigen-antibody complex with this one type
Placebo benefits
Prevents psycology bias
Prevents bias from medical professionals and researchers
HIV
Human Immunodeficiency Virus
AIDS
Acquired Immune Deficiency Syndrome
Structure of HIV
HIV RNA: two identical single stranded RNA molecules containing the genetic material for making more HIV particles
Reverse Transcriptase: 2 copies of this enzyme that transcribe the RNA into host DNA once inside the cell
Viral envelope: Piece of the plasma membrane budded off the last T helper host cell (phospholipid)
Capsid: Bullet shaped protein coat that protects the HIV RNA within
Surface glycoproteins: Protein spikes that allow HIV to attach to CD4 receptors on host T helper cell due to complementary shape
How does HIV replicate
- Protein on HIV binds to CD4 receptor protein on T helper cell membrane
- Capsid fuses with its plasma cell membrane and releases viral mRNA and enzymes into Th cell
- Reverse transcriptase converts viral mRNA into cDNA using host nucleotides
- Viral cDNA moves into nucleus of Th cell and is inserted into the host genome
- Person is now infected
- Translation of this produces mRNA, then translated so the cell starts to manufacture HIV particles
- Particles break away from host cell with some of the host cells surface membrane
- Which forms the viral lipid envelope
- Over time leads to a reduction in the number of Th cells by inactivation of Th cells
How can you tell if someone has HIV or AIDS
Uninfected healthy person should have 800-1200 Th cells per mm cubed of blood
If suffering with AIDS, can be as few as 200
Screening for HIV can detect and determine HIV status of patient
AIDS isn’t a pathogen so can’t be detected with antigens or antibodies
AIDS screened for by checking the number of Th cells
Relationship between HIV and AIDS
HIV causes AIDS
What is AIDS
Caused by HIV
Leaving victims vulnerable to secondary diseases and opportunistic infections
Symptoms of AIDS
Pneumonia
Kaposi’s sarcoma (connective tissue cancer)
Weight loss
Diarrhoea
Can develop lung, intestine, brain or eye infections
What are antibiotics
Drugs prescribed to treat bacterial infections
How do antibiotics work
Prevent bacteria making a normal cell wall of peptidoglycan
So bacteria can’t resist osmotic pressure
Cells burst due to an increase in water volume by osmosis
Why don’t antibiotics work on viruses
Virus uses host cell organelles to carry out metabolic activities so no viral organelles to disrupt
Since usually in host cell they are out of reach of antibiotics
Have a capsid not murein cell wall which does not allow antibiotics to act on viruses as they do bacteria
How can HIV lead to death
Doesn’t directly kill but compromises the immune system and leaves people vulnerable to secondary diseases and opportunistic infections that ultimately cause death
B memory cells must be activated by Th cells, which may have been destroyed therefore can’t carry out a secondary immune response
What are T cells and why are they called that
T lymphocytes
Responsible for the stage in the immune system called the cellular response
Primarily produced in the thymus
What are B cells and why are they called that
B lymphocytes
Type of leukocyte responsible for producing and releasing antibodies in the humoral response
Produced in the bone marrow
Active natural immunity
Immune after catching a disease
Active artificial immunity
Immune after vaccine
Passive natural immunity
Body immune from antibodies from placenta/breast milk
Passive artificial immunity
Immune after injected with antibodies from someone else/monoclonal antibodies
Full function of memory cells
Remain in circulation in case of future reinfection of the same pathogen
If they encounter the antigen again they are rapidly activated by cytokines secreted by specific Th cells and rapidly divide by mitosis
Producing lots of antibodies in a short time frame
Latent
Virus is there but doesn’t replicate
Viron
Infectious virus particle that can enter host cell and replicate
Retrovirus
Single stranded RNA inside virus
