Immunology Vaccinations and Hypersensitivity

Passive Immunity

• The transfer of preformed antibodies to recipient

• Temporary

• No memory

• Maternal IgG antibodies from placenta

• Maternal IgA from milk

• Monoclonal therapy

• Antitoxins

Active Immunity

• Immune system develops own response

• Vaccination or infection

Primary Immune response

• First encounter w antigen

• Generates plasma cells and memory cells

• slow

Secondary Immune response

• Re-exposure to antigen

• Memory cells respond fast

• Quick and Concentrated amounts of high affinity antibody production

What’s about antigen is considered for Vaccine Design

1. Accessibility to immune system

2. Essential for pathogen function, survival, and evolution

3. Stable

4. Stimulates B and T cells

5. Not similar to host

What’s and adjuvant

• substance added to antigen or vaccine to increase immune response

• increased immunogenicity

• localized inflammation

• prolonged exposure

• lymphocyte activation

What is a live attenuated vaccine

• Weakened pathogen that can still replicate

• Mimics infection

• Strong CD4 and CD8 response

• Risky

What is an inactivated vaccine

• Killed pathogens that cant reproduce

• Processed on MHC 1 to CD8 t cell

• Needs booster

Subunit Vaccine

• Part of pathogen thats immunogenic

• Needs adjuvants

Polysaccharide Vaccine

• Peptidoglycans or sugars are used

• Mainly activates

Conjugate Vaccines

• Helps chilren respond to polysaccharide based vaccines

• Links sugar to protein / hapten carrier

Recombinant Protein vaccines

• Protein antigens from recombinant DNA

• Multiple doses

mRNA Vaccines

• Use part of pathogens genome that codes for pathogenic protein

• Nano-Particle transport

• Antigen processed on MHC 1 to CD8 and B Cell response

Viral Vector Vaccines

• Like mRNA but uses virus as transport

Type 1 Hypersensitivity

• Genetic

• Allergies and Barrier disruption

• IgE cross-linking (many AB connects to one AG)

• Mast cell degranulation

• Th2 T helper cells response

Type 1 effector response

1. APC presents exogenous AG to Th2 helper cells on MHC2

2. Th2 releases IL-4 / IL-12

3. Plasma cells made

4. IgE secreted and binds to mast cells FC receptors for weeks

5. Crosslinks AG

6. prostaglandins made

7. prolonged response by cytokines, eosinophils, basophils, and Th2

8. Inflammation and tissue damage

what is Atopy

genetic predisposition to IgE and TH2 response to allergens

Weak barrier function from defective filaggrin gene

Type 2 hypersensitivity

• IgG and IgM

• eg… blood transfusions, hemolytic disease in pregnancies, thyroid disease

• Neutralization

• Complement, NK cells, neutralization

Type 3 hypersensitivity

• Immune complex build up

• IgG IgM

• Chronic localized inflammation

• tissue damage

• Lupus, bruising, serum sickness

type 4 delayed hypersensitivity

• Only cell mediated hypersensitivity

• Th1 T cells and CD8

• slow, 1-2 weeks before symptoms

• Hapten chemicals and metals cause activation

• Lesions, inflammation, contact dermatitis, Tuberculosis granulomas (similar to neutralization but with macrophages and T cells surrounding retro infected cells)

type 4 effector response

1. APCs phagocytose AG and present to helper cells on MHC2

2. IL-12 released from APCs and drives TH1 response

3. Th1 form memory cells

4. Re-exposure

5. Th1 presented AG on MHC2

6. secrete cytokines that recruit macrophages

7. Localized Tissue damage