Unit 8: Adaptive immunity

Antigens

found on pathogens and can stimulate the immune system

Bacterial antigens

capsule, fijmbraie, flagella, cell walls, etc

Viral antigens

spikes, envelopes, fibers, etc

Epitopes

specific regions on antigen where antibodies bind to

Types of antigens

protein, carbohydrate, lipid, DNA

Protein antigens

more potent antigens

Carbohydrate antigens

antigens that can only stimulate the humoral immune defence

Lipid and DNA antigens

the least antigenic antigens

Antibodies

immunoglobulins, produced by immune system to target antigens
- IgG, IgM, IgA, IgD, IgE

IgG

most abundant antibody in the body

IgA

antibody found in respiratory secretions

IgE

antibody that aids in allergic responses and defence against parasites

Cellular immunity

- involves T cells
- main target is to kill infected body cells + boost overall immune response

Humoral immunity

- involves B cells
- main target is to kill extracellular antigens by producing antibodies

Formation of T cell library

hematopoietic cells formed in bone marrow
> half migrate to thymus = naive T cells

Naive helper T cells

contain
- T-cell receptor (TCR)
- CD4 co-receptor

T-cell receptor (TCR)

receptor on T cells capable of binding to a specific epitope

Naive cytotoxic T cells

contain
- TCR
- CD8 co-receptor

Activation of naive helper T cells

1. pathogen/antigen phagocytosed
2. protein complex MHC-II combines with antigens; recognition
3. MHC-II + antigens presented on cell membrane
4. macrophage > APC
5. TCR on naive helper T binds to displayed antigen
6. CD4 on naive helper T binds to displayed antigen, anchors
7. APC + helper T release cytokines, activate naive helper T
8. naive helper T proliferates and differentiates

Differentiations of naive helper T cells

- T helper 1
- T helper 2
- memory T cells

T helper 1 (TH1)

stimulate other cells in immune response

T helper 2 (TH2)

function to stimulate the humoral immunity

Memory T cells

function to remember the antigen
- if same antigen encountered again, cell will switch to either TH1 or TH2

Cytotoxic T cell activation

same way as helper T but:
- MHC-I not MHC-II
- anchoring done by CD8
- naive > effector + memory T cells

Differentiations of naive cytotoxic T cells

- effector cytotoxic T cells
- memory cytotoxic T cells

Effector cytotoxic T cells

once activated, will release perforin and granzymes

Perforin

released by effector cytotoxic T cells, create pores in the target cell

Granzymes

released by effector cytotoxic T cells, proteases while enter the pores and induce apoptosis

Formation of B cell library

hematopoietic cells formed in bone marrow
> half stay in bone marrow and become B cells

B cells

each coated with IgM antibodies, capable of binding to a single epitope

TH2-dependent B cell activation

1. IgM antibodies of inactive B cell bind to foreign antigen
2. IgM-antigen complex internalized into inactive B
3. antigen combines with MHC-II and presented onto B cell plasma membrane
4. B cell > APC
5. matching TH2 cell binds to antigen
6. TH2 cell releases cytokine > activates B
7. B cell proliferates and differentiates

Differentiations of TH2- dependent naive B cells

- plasma cells
- memory B cells

Plasma cells

secrete IgM antibodies initially, then longer-lasting IgG

Memory B cells

remember the antigen; switch to plasma cells if antigen encountered again

TH2-independent B cell activation

1. occurs with T-independent antigens
2. B cell directly activated through binding of IgM antibody to foreign antigen
3. once activated, B cell proliferates + differentiates into only plasma cells
= shorter-lived response

Actions of antibodies

- neutralization
- opsonization
- agglutination
- complement cascade activation
- Ab-dependent cell-mediated toxicity

Neutralization

the binding of antibodies to epitopes to prevent attachment to cells

Opsonization

the coating of a pathogen to enhance phagocytosis

Agglutination

the cross-linking of antigens to create large clumps

Antibody-dependent cell-mediated toxicity

enhanced killing of pathogens that are too large to be phagocytosed

Active immunity

the activation of an individual's own immune defences

Active, natural immunity

immunity gained through illness and recovery

Active, artificial immunity

immunity through vaccinations

Passive immunity

the transfer of adaptive immune defences from another individual or animal

Passive, natural immunity

antibodies passed through breast milk or placenta

Passive, artificial immunity

transfer or antibodies harvested from an individual or animal

Herd immunity

when there are too few susceptible individuals for a disease to spread effectively
ex. vaccination programs

Vaccinations

the deliberate exposure of a person to an antigen to trigger a primary response without feeling the effects of the pathogen
> secondary response occurs when they actually encounter the pathogen

Types of vaccines

- live attenuated
- inactivated dead
- subunit
- toxoid
- conjugate
- nucleic acid

Live attenuated vaccines

weakened organisms; can still replicate so boosters not needed
- increased challenges for storage + transport
- ex. chicken pox

Inactivated dead vaccines

no risk of severe infections, but boosters needed often
- useful for vaccination programs
- ex. influenza shot

Subunit vaccines

contains only the key antigens of a pathogen
- produced through genetic engineering or isolation from degraded pathogen
- no protection against antigenic variation
- ex. hep B, HPV

Toxoid vaccines

contain inactivated toxins; pathogens themselves not included
- least amount of side effects, but does not prevent infection
- ex. botulism, tetanus, pertussis

Conjugate vaccines

synthetic vaccines that combine carbohydrate antigens with larger protein to stimulate both cellular and humoral immunity
- more expensive
- ex. meningitis

Nucleic acid vaccines

nucleic acid is injected cells take up the nucleic acid and use it as a template to make protein antigens
- ex. COVID