microbes and the immune system Flashcards
(85 cards)
1
Q
symbiosis
A
= symbiotic relationship involves the association of 2 or more partners
2
Q
symbiotic relationship
mutualism
A
= both organisms benefit.
bacteria examples:
- colonic bacteria provided with a niche in the host
- Ruminococcus spp. can be found in high numbers in the gut and involved in cellulose breakdown.
fungi examples:
- fungi attach to the roots and allow root extension, in exchange the plant provides sugars to the fungi.
3
Q
commensalism
A
= one organism benefits and the other neither benefits or is harmed.
example: - Staphylococcus epidermidis utilises dead skin cells without causing harm
4
Q
parasitism
A
= one organism benefits at the expense of the other
- parasitic microbe lives or multiplies within/on the host, causing damage in the process
example: malaria -> plasmodium falciparum
5
Q
opportunistic pathogen
A
a pathogen that does not normally cause disease, only causes disease when the host’s defences are compromised
example: cold sores - herpes simplex virus
6
Q
primary pathogen
A
can cause disease in a host regardless of the host’s immune system state, or barriers.
7
Q
Koch’s postulates- traditional
A
= koch’s postulates are a set of criteria that establish whether a particular organism is the cause of a particular disease.
traditional states that:
- pathogen must be absent in all healthy individuals but present in all diseased hosts.
- pathogen must be isolated and grown in pure culture
- it must cause the same disease if introduced into a healthy host
limitations:
assumes all organisms can be cultured in a lab
ethical issues infecting healthy hosts ]
doesnt explain disease caused by multiple pathogens or pathogens that can live in healthy hosts
8
Q
modern Koch’s postulates
A
- isolation of genetic material enables pathogen identification
- specific genes correlate with disease
- used to determine what genes contribute to a pathogen’s ability to cause disease
- some pathogens can exist in healthy individuals which conflicts the traditional way.
9
Q
what is pathogenicity, phenotypic switching and virulence?
A
pathogenicity = the ability to cause disease
virulence = the degree of pathogenicity of an organism (infectvity/ intensity)
phenotypic switching = changing appearance depending on the environment it is in, increased invasion as can get passed the defense in alternative form.
10
Q
identification tools for microbes
A
1.) agar plates (culture method, however is not suitable for all organisms)
2.) molecular techniques (OMICS)
- genomics (can identify genes and organisms from DNA)
- transcriptomics( tells you parts of DNA that have been expressed, to allow protein production from RNA)
- proteomics( what proteins are produced)
- metabolics( metabolites produced by a population living together)
3,) microarray technology ( tells you what genes are expressed within each population using florescence, a general laboratory technique)
11
Q
viral replication process
A
1.) attatchment of virus to host cell through specific receptors
2. virus enters host cell
3. the viral genome is replicated
4. viral genomes are transcribed and translated by host cells ribosome (gene expression)
5. assembly of viral genomes and proteins
6. release from host cell, to infect new cells.
12
Q
genetic properties of RNA
A
- uses uracil instead of thymine
- nuclear and cytoplasmic
- OH at 2’ ribose position
- short term storage
- small genome size
- low intrinsic stability ( reactive to neighbouring dipoles)
- single stranded (either a positive or negative strand)
- low polymerase fidelity (ability to replicate a template)
- low error correction
13
Q
genetic properties of DNA
A
- uses thymine
- mainly found in nucleus
- H at ribose 2’ (no oxygen)
- long term storage
- high intrinsic stability (less reactive, cos no O)
- large genome size
- high polymerase fidelity
- high error correction
14
Q
differences between DNA and RNA viruses in terms of: genome size & organisation; infection cycle; antigenic drift and shift; recombination & mimicry; latency
A
Genome: DNA viruses have larger, stable genomes; RNA viruses have smaller, mutation-prone genomes.
Infection Cycle: DNA viruses often replicate in the nucleus, RNA viruses usually in the cytoplasm.
Antigenic Variation: RNA viruses exhibit frequent antigenic drift and more opportunities for antigenic shift.
Recombination & Mimicry: Both types can recombine and mimic host molecules, but mechanisms differ.
Latency: DNA viruses are more likely to establish long-term latency, while RNA viruses are typically associated with acute infections.
Antigenic shift and drift: RNA viruses are more prone to these changes due to their high mutation rates and segmented genomes.
RNA viruses have faster evolution capacity -> rapid adaptation, they also have greater coding capacity
15
Q
antigenic shift
A
= a major alteration in antigen sequence by a process of genome reassortment (segmented virus) or inner strain recombination that results in a new strain of the virus. (sudden change in genetic makeup)
16
Q
antigenic drift
A
- virus undergoes a gradual change in genetic makeup, causing a different, but somewhat similar genetic makeup to the parent virus.
- antigens accumulate small mutations, is these are advantageous, will become predominant through selective pressures
17
Q
segmented virus
A
Viruses that packages all of their genome segments into a single particle. This allows the virus to be infective.
- they can have multiple segments ( encoded genes are divided across molecules of DNA or RNA)
18
Q
recombination
A
= allows for major alterations through exchange of genetic material between viruses or with the host
- genetic exchanges between a pair of homologous DNA sequences
19
Q
viral mimicry
A
= stealing from the host
- can disable the immune system with decoys which is:
- favoured by the large size of DNA viral genomes
- favoured by DNA-DNA host virus recombination
20
Q
latency
A
=state where a virus remains dormant or inactive within a host cell for an extended period, without actively replicating or causing disease symptoms ( absence of antigens)
- long lived nature of DNA allows for long lasting infections
- DNA viruses are more difficult to detect in nucleus -> persistent infections through latency
- a lack of immune response to infected cells in latent state
- clinical consequence -> recurrent infections
21
Q
what happens when virus’ undergo mutations
A
= Mutation in viruses (coping errors during replication) - lead to alterations in the virus’ surface proteins or antigens. Our immune system uses these antigens to recognize and fight the virus.
22
Q
what drives bacterial genetic change?
replication
A
- evolution in bacteria is rapid due to their high replication rates
- E.coli can double in number every 25 minutes under optimal growth conditions
23
Q
what drives bacterial genetic change?
mutation
A
- can alter efficacy of antibiotic by altering the target site
- can alter the receptor recognition of tissue host
- can alter the recognition by the host for the pathogen
- can lead to antigenic drift, where minor changes in surface proteins help the virus evade immune recognition.
24
Q
what drives bacterial genetic change?
horizontal gene transfer
A
= accquiring new genetic traits in bacteria through DNA exchange between two bacteria
3 types:
natural transformation = DNA from the environment is taken up and incorporated into the bacterial chromosome by homologous recombination.
Conjugation = genetic exchange between bacteria
Transduction = genetic exchange occurs through predation by bacteriophage. These are small viruses of bacteria that inject DNA into the cells as part of replication cycle.
25
# what drives bacterial genetic change?
transformation
= occurs in bacteria that are naturally competent. ( able to actively transport environmental DNA fragments across their cell envelope and into their cytoplasm)
- occurs when DNA is released during bacterial lysis. (when bacteria die and lyse)
- involves bacteria taking up and incorporating free DNA into their genome from the environment.
- they do this through homologous recombination.
26
# what drives bacterial genetic change
conjugation
= bacterial sex (direct exchange of DNA)
- occurs between two conjugative plasmids which carry the genes for building the pilus structure and ensuring DNA is transfered.
A bacterium with a conjugative plasmid (called F+ bacterium) forms an F pilus on its surface.
The pilus attaches to a bacterium lacking the plasmid (F- bacterium).
The pilus pulls the two bacteria together, creating a mating bridge.
The conjugative plasmid is then transferred through this bridge from the donor to the recipient.
27
# what drives bacterial genetic change
transduction
- bacteriophages can adopt to two life cycles:
1.) lytic cycle = replication of bacterial genome and destruction of bacteria. (attachment, penetration, replication, packaging, and burst out)
2.) lysogenic = integration of the bacteriophage DNA into the bacterial chromosome
28
key difference between lytic and lysogenic cycle
Lytic Cycle: bacteria destroys the host immediately.
Lysogenic Cycle: Bacteria integrates into the host and stays dormant, potentially switching to the lytic phase later.
29
pathogenicity islands
= large pieces of DNA that encode multiple genes are integrated into the chromosome. These large island regions can encode multiple genes for different structures.
Foreign DNA that’s inserted into bacterial chromosome is identified by their difference in guanine and cytosine content.
30
the two types of communication in bacteria
Quorum sensing = results in changes in gene expression as a consequence of signalling at the population level.
- Occurs when bacteria sense their population size and coordinating their behaviour in response
- behaviour changes depend on bacterial cell density
- low density = no transcription of target gene
- high density = transcription occurs
Environmental sensing = results in changes to gene expression within an individual bacterium
- relies on interaction between two proteins in response to particular stimulus.
31
31
the two component regulation of environmental sensing
component 1 = transmembrane sensor kinase
- sensory domain on outside of cell
- kinase domain protrudes into the cytoplasm
- on detection of a signal -> conformational change in kinase domain -> autophosphorylation.
component 2 = response regulator
- trans phosphorylated by the kinase
- this acts to enhance or repress gene expression of one or more genes.
32
transcriptomics
= can use to study the capacity of bacteria to modify gene expression in response to environmental conditions.
this allows us to identify those genes whose expression are essential for growth within a niche.
33
generalized vs specialised transduction
Generalized: Random bacterial DNA incorporated into defective phages.
Specialized: Adjacent bacterial DNA excised with phage DNA. ( bacteria can only pick up specific portions of hosts DNA)
34
# microbial life strategies to obtain energy and carbon
photoautotrophs
Use sunlight and carbon dioxide (CO2) for energy
examples: plants, algae, and cyanobacteria.
35
# microbial life strategies to obtain energy and carbon
chemoautotrophs
Obtain energy through chemical oxidation and use CO2 as their carbon source, typically found in extremophiles.
36
# microbial life strategies to obtain energy and carbon
photoheterotrophs
they use sunlight for energy but rely on pre-formed organic compounds for carbon.
Examples are purple and green non-sulphur bacteria
37
# microbial life strategies to obtain energy and carbon
chemoheterotrophs
Depend on chemical oxidation for energy, obtain their carbon from pre-formed organic compounds.
- animals and humans
38
temperature adaptations of psychophiles, hyperthermophiles and mesophiles
Psychrophiles thrive in cold environments, with growth optimal at <15ºC. They adapt by increasing unsaturated fats in their membranes to maintain fluidity.
Hyperthermophiles require high temperatures >70ºC for survival, adapting by increasing saturated fats in their membranes to maintain structural integrity.
Mesophiles grow best at body temperature (37ºC) and are often human pathogens.
39
microbes in the marine environment
neritic zone = mild temperatures, low pressure, nutrient rich and home to diverse marine life such as photosynthetic organisms.
oceanic zone = high pressure and deep water environments where chemotrophs thrive.
Ocean plankton, especially species like Prochlorococcus and Synechococcus, are critical for Earth's oxygen production and carbon fixation.
40
how are microbes used in technology?
PCR = Uses Taq polymerase from Thermus aquaticus to amplify DNA, transforming molecular biology.
Restriction Enzymes = Bacterial proteins that cleave DNA at specific sequences, fundamental in recombinant gene technology.
CRISPR-Cas9: A bacterial immune system that can be harnessed for precise gene editing by targeting specific DNA sequences.
41
how are microbes used in medicine?
antibiotics = Penicillin, discovered from Penicillium notatum, was the first broad-spectrum antibiotic, inhibiting cell wall synthesis in bacteria.
Recombinant Vaccines: Use microbial methods to express antigens (e.g., hepatitis B surface antigen in yeast) to produce vaccines.
Recombinant Virus Vaccines: For COVID-19, spike protein genes were inserted into harmless viruses to trigger immune responses in the body.
42
microbes and cancer
Certain microbes are implicated in cancer development:
Human papillomavirus (HPV): Associated with cervical cancer.
Helicobacter pylori: Linked to gastric cancer.
Schistosoma haematobium: Linked to bladder cancer.
43
biodegradation by microbes
= the physical or chemical change of a material by micro-organism(bacteria, fungi)
plastics can impact the microbiome by having toxic effects and providing a platform for colonisation.
44
What role do cryoprotectants and cold/heat shock proteins play in microbial survival?
They prevent proteins from denaturing and help maintain proper structure and activity under extreme temperature conditions.
45
describe the methods that have revolutionised the microbiome field
- many bacteria are still not culturable so sequencing is used:
1.) 16S sequencing = Targets a specific region of rRNA to identify bacteria. cost effective
2.) Whole genome sequencing(WGS) = sequences the entire genome including non coding and coding protein regions. More comprehensive than 16S but high costs.
3.) metagenomics = the study of the structure and function of entire nucleotide sequences
46
describe how communities of micr-organisms colonise us
- by the time we are 3 years old our microbiomes are largely established and remain relatively stable throughout life.
- our bodies are around 50% bacteria, with different bacterial communities colonisisng different body surfaces.
- these communities are complex, stable and interdependent.
- Factors like pet ownership, maternal health, diet and genetics affect microbial colonization.
- bacteria help in processes like micronutrient synthesis and limit pathogen colonization.
47
how are microbial communities important for ourr health?
- bacteria synthesis essential micronutrients such as vitamin K and biotin.
- they metabolize plant carbohydrates into short chain fatty acids which provide energy to epithelial cells.
- short chain fatty acids are produced by bacterial fermentation, including butyrate (has anti-inflammatory effects), acetate and propionate.
- probiotics have limited evidence of efficacy but are generally safe.
48
describe how the microbiota contribute to disease
Inflammatory bowel disease = Includes conditions like ulcerative and Crohn's disease. Disease is influenced by interplay between the microbiome, genetic factors and the immune system(innate and adaptive).
- infiltration of bacteria drives inflammation.
Clostridium dificile infection = A bacterial infection that causes gastrointestinal issues. It can spread via contaminated surfaces and release toxins that damage the colon and may lead to pseudo membrane formation.
49
the immune systems initial response to infection
- activation of innate immune cells, increased permeability of blood vessels and migration of immune cells to the site of infection leading to acute inflammation.
key immune cells involved: dendrites, macrophages and mast cells which are found in tissues.
50
how does the immune system recognize harmful pathogens from harmless substances
= by pathogen associated molecular patterns(PAMPS)
Pattern recognition receptors(PRR) recognize PAMPS and these are specific to different pathogens:
Toll like receptors (TLR) -> recognise various PAMPS
nucleotide binding oligomerisation domain like receptors(NLR) -> recognise range of PAMPS and DAMPS.
C-Type Lectin Receptors (CLRs): Recognize pathogen carbohydrates, often used to detect fungi.
Retinoic Acid-Inducible Gene I-like Receptors (RLRs): Detect viral RNA (single-stranded and double-stranded).
Absent in Melanoma 2-like Receptors (ALRs): Recognize bacterial and viral cytoplasmic DNA.
51
how some pathogens can evade detection
polio virus: hides from PRRs by stealing RNA caps from host mRNA
Helicobacter pylori: Evades TLR5 recognition by flagellin modification.
52
the danger model and DAMPs
danger model = immune responses are triggered by damage or danger rather than pathogens just being 'non self'.
DAMPs = damage associated molecular patterns
- they indicate cellular damage resulting from infection
- such as nucleic acids, metabolites and nuclear proteins which are released from dying cells.
53
complement system
= a series of plasma proteins that act in an enzymatic cascade to control pathogens.
- some pathogens and host cells evade the complement system by using inhibitors such as CD46 which inactivates C3b, CD59 which stops MAC from forming, C1 inhibitors and proteins like SPICE from smallpox.
the main complement mediators:
C3b: Binds to pathogens and marks them for destruction (opsonization).
C5a: Acts as a potent inflammatory mediator that attracts immune cells.
MAC (C5b-C9): Creates pores in the pathogen membrane, causing it to burst.
Complement proteins help immune cells recognize, attack, and kill pathogens more efficiently.
54
different PAMPs found on pathogens
Bacteria: Cell wall components, bacterial DNA
Viruses: Viral nucleic acids, glycoproteins
Fungi: Polysaccharides
Protozoa: Glycolipids
55
consequences of pattern recognition receptor activation
1. tell neighbouring cells about the threat -> makes inflammatory cytokines
2. tells the adaptive immune system -> phagocytose the microbe and take it to the draining lymph node
3. limit microbe replication -> control pathogen
56
consequences of microbial sensing for the host
1. altered gene expression:
Bacteria trigger gene changes by activating NF-κB.
TLR activation starts a process that activates NF-κB.
NF-κB moves into the nucleus and changes gene activity.
This helps the cell alert the immune system about the infection.
Some pathogens, like E. coli, can reduce NF-κB activation to avoid signaling the immune system.
57
appreciating the scale and magnitude of antibiotic resistance
Infections were the leading cause of death until the 1960s when antibiotics were introduced, revolutionizing healthcare.
Antibiotic resistance affects all countries, but poverty and inequality worsen its impact.
Antibiotic resistance directly caused 1.27 million deaths globally in 2019, and contributed to an additional 4.95 million deaths.
58
what are the causes of antibiotic resistance
- over prescribing of antibiotics
- patients not finishing their treatments
- overuse of antibiotics in livestock and fish farming
- poor infection control in hospitals and clinics
- lack of hygiene and poor sanitation
- lack of new antibiotics being developed
overprescribing:
- Excessive use of antibiotics in humans leads to bacteria encountering the drugs, increasing the chances of resistance.
- To combat this, global efforts should focus on public education, better diagnostic tools, and stricter regulations.
not finishing treatment:
- When patients don't finish their antibiotic courses, bacteria can survive, multiply, and mutate, increasing the risk of resistance
59
how do antibiotics work?
their main targets:
1. nucleic acid synthesis (targetting DNA and RNA production)
2. ribosomal function (disrupting protein production)
3. cell wall (preventing the formation of the bacterial cell wall)
4. cell membrane (damaging the plasma membrane)
5. inhibition of cell metabolism and growth (inhibits key metabolic pathways)
60
B lactam antibiotics
Target penicillin-binding proteins (PBPs) in bacteria, preventing the cross-linking of the cell wall, causing the bacteria to burst.
61
what are the two types of antibiotic resistance
1. intrinsic = ome bacteria are naturally resistant to certain antibiotics due to their structure or physiology.
2. acquired = Bacteria can gain resistance through mutations or by acquiring resistance genes from other bacteria.
62
mechanisms of antibiotic resistance
1. reduced drug uptake = bacteria prevent antibiotics from entering
2. enzymatic degradation = bacteria produce enzymes that break down antibiotics
3. target modification = bacteria modify the antibiotics target making it ineffective.
4. increased drug influx = bacteria pump antibiotics out faster than they can enter.
63
how quicky does antibiotic resistance develop?
= this depends on how much of the antibiotic is being used
- overuse accelerates resistance.
64
what is being done to tackle antibiotic resistance?
- drugs
- diagnostics
- surveillance
- vaccines
- new therapies
- infection control
65
when was the golden era of antibiotic discovery
1940s to 1960s
66
what are the ways in which parasites evade destruction by the immune system?
1.) avoidance by location
- hiding in host cells
- plasmodium hide in the liver and red blood cells
- toxoplasma hide inside macrophages
- T cruzi hide in neurons, muscles and macrophages
2.) Encapsulation in cysts (closed sac like structures)
- toxoplasma: form cyst tissue
3.) Antigenic mimicry
- parasites mimic the host antigen to confuse the immune system
- schistoma mimic blood group antigens
4.) immunosuppression
- suppression of host immune responses, so it cannot fight infection and disease
- T cruzi, T brucei, filarial worms and schistomas do this
5.) antigenic variation
- alternation of surface antigens to avoid antibody detection
- Examples: Trypanosoma brucei, Borrelia (Lyme disease), Plasmodium (malaria), and Neisseria (gonorrhea).
67
explain the process of antigenic variation by the African trypanosomes
- African trypanosomiasis is caused by trypanosoma brucei and transmitted by tsetse flies.
- Parasite surface coated with Variant Surface Glycoprotein (VSG).
the mechanisms;
1.) gene conversion
- the parasites have 1000+ VSG genes stored in a silient genomic pool.
- only one VSG is expressed at a time
2.) Switching VSG expression
- host immune system can express antibodies that target the VSG gene
- the parasite can switch to a different VSG, through genetic recombination, relplacing the active VSG with a silient one
3.) immune evasion
- parasite can constantly change its coat, avoiding immune evasion
- results in chronic infection.
mono- allelic expression
- only one VSG expressed at a time via the expression site body
- switching involves either moving a new VSG into the expression site body or activating a different expression site body.
68
describe the host immune response to Helminths and their immunosupressive mechanisms
helminths are large worms that are too big for phagocytosis, so require specialised processes
1.) immune response:
- IgE-mediated response = IgE bind to helminths and recruits eosinophils, eosinophils release toxic proteins that can damage the worm.
2.) immunosuppressive mechanism
- helminths can suppress host immunity to reduce tissue damage
- regulatory T cells diminish inflammation (regulatory T network)
- they can secrete immunomodulatory molecules to suppress immune responses.
69
the hygiene hypothesis
- Lack of helminth infections in developed countries may explain increased allergies and autoimmune diseases.
Helminths "train" the immune system to suppress inappropriate responses:
Allergies (e.g., pollen, dust mites).
Autoimmune diseases (e.g., rheumatoid arthritis).
70
Exploiting Helminth-Derived Molecules for Therapy
Example: ES-62 protein from Acanthocheilonema viteae (a rodent helminth):
Reduces inflammation and ameliorates autoimmune diseases.
Challenges: Direct use of ES-62 triggers immune responses.
Solution: Small chemical analogs of ES-62 are under development as anti-inflammatory drugs. (mimics proteins activity)
71
the cellular basis of immunological memory
Vaccines help stimulate the immune system to remember a pathogen, allowing for faster and stronger responses if the body encounters the same pathogen again.
72
memory vs naive B lymphocytes
- memory B cells are:
-long lived
increased frequency
rapid proliferation
produce more antibodies
produce higher affinity antibodies
memory cells are more efficient than naive b cells which have not been exposed to the antigen yet.
73
memory vs naive T lymphocytes
memory T cells;
- long lived
- increased frequency
- rapid proliferation
- lower activation threshold
- better effector function
naive t cells are precursors for effector and memory T cells.
T-cell Vaccines:
Cytotoxic T-lymphocytes kill infected cells, such as those infected by the influenza virus.
74
why are secondary responses better?
germinal centre maturation drives affinity maturation and class switching of memory b cells and long lived plasma cells.
vaccines can work by inducing long lived plasma cells that promote long lasting antibody responses.
75
How Vaccines Exploit Memory and Eliminate Infectious Disease
| herd immunity and immunisations
vaccine herd immunity = minimum threshold of a population that need to be vaccinated to offer protection foe those who are not, to limit disease spreading.
Routine UK immunisations=
killed (influenza)
live, attentuated (measles, shingles)
76
the stategies used to make vaccines
1.) virus attenuation
- making a virus less harmful to stimulate a strong and long lasting immune response.
- example sabin polio vaccine
2.) killed vaccines
- Made from proteins or small pieces of a virus or bacterium that are killed via chemicals or heat, making them non-infective but still capable of stimulating immunity.
Example: Whole cell pertussis vaccine.
3.) subunit vaccines
- Made from components of a pathogen (e.g., bacterial toxins) that are incapable of causing disease but stimulate an immune response.
Toxins can be inactivated to produce toxoid vaccines.
Example: Acellular pertussis vaccine.
4.) recombinant subunit vaccines
- Contains purified parts of the pathogen necessary to induce a protective immune response.
Examples: Human papillomavirus (HPV) vaccine.
5.) live/ attenuated influenza virus
- vaccines for the prevention of influenza disease
- effective in children over 2, ineffective in over 50s
77
the vaccine design process
Antigen Identification: Identifying the right antigens to stimulate the immune response.
Vaccine Delivery: Ensuring the vaccine is delivered effectively to the body.
Immune Activation: Activating the immune system to generate a protective response.
adjuvants = agents which act non specifically to increase the specific immune response or response to the antigen.
78
what is adaptive immunity
= the part of the immune system that is specifically tailored to recognize and fight off pathogens, using specialized cells and receptors. It provides long-lasting immunity after exposure to a pathogen, with the ability to "remember" previous infections.
79
the main cell types of the adaptive immune system
cellular adaptive immunity (T cells):
- CD4 T cells (helper T cells that assist other immune cells by releasing cytokines)
- CD8 T cells (killer T cells, kill by releasing toxins)
humoral adaptive immunity:
B cells that produce antibodies to help neutralize and fight off pathogens.
These cells have unique receptors (BCR for B cells and TCR for T cells) that allow them to specifically recognize antigens.
80
how is adaptive immunity activated
1.) B cell activation
- B cells recognise native antigens through their b cell receptor (BCR), No accessory cells are needed for this activation.
2.) T cell activation
- t cells recognise processed antigens presented on MHC molecules by antigen presenting cells
- CD8 T cells recognize antigens presented by MHC class 1
- CD4 T cells recognize antigens presented by MHC class II.
- t cell activation requires 3 signals: antigen presentation, co-stimmulatory molecules and inflammatory cytokines.
- activated T cells undergo colonal selection and clonal expansion to fight the pathogen.
- both take place in secondary lymphoid organs. (lymph nodes and spleen)
81
subsets of T helper cells
thelper 1 cells;
- Respond to viral and intracellular bacterial infections. They release IFNγ and TNF to enhance the innate immune response.
thelper 2 cells;
- Help with responses to helminths (parasitic worms) and promote wound healing by releasing IL-4 and IL-5.
thelper 17 cells;
- Activate neutrophils and produce antimicrobial molecules to fight fungi and extracellular bacteria.
82
B cells response and antibody production
- b cells produce antibodies that help to neutralise pathogens, activate complement and enhance phagocytosis.
- somatic hypermutation and class switching of b cells leads to higher affinity antibodies and different types of antibodies such as IgM, IgG and IgE.
- plasma cells can produce large quantities of antibodies.
83
CD8 t killer cells mechanism
- release perforin to create pores in tatget cell membranes
- release granzymes to trigger apoptosis in infected cells
- produce inflammatory cytokines to enhance immune response.
84
how antibodies protect the host
neutralization: block toxins or viruses from bidning to the host
complement activation: trigger the complement cascade, leading to pathogen lysis.
opsonization: mark pathogens for phagocytosis by macrophages and neutrophils.
