10- Hypersensitivity Flashcards
What is an allergen?
***An antigen that stimulates IgE production
Small, highly soluble molecules carried on other particles that come into contact with mucus membranes, elite, and diffuse through (attach themselves to things, triggering response)
What is atopy?
The INCREASED TENDENCY seen in some people to produce immediate hypersensitivity reactions against innocuous substances
What is type 1 hypersensitivity? And it’s common name? What is responsible for it?
Common name: immediate hypersensitivity (“real” allergies)
Responsible: TH2, IgE antibodies, mast cells, eosinophils
Antibodies and IgE–> triggers mast cell degranulation (what person feels during allergic response)
Type 2 hypersensitivity? Responsible? Common name?
Common: antibody-mediated diseases, cytotoxic
Responsible: IgM and IgG
Cytotoxic because antibodies will bind to self targets and trigger destruction
What is an allergic reaction? What type of hypersensitivity?
A harmful immune reaction to an inherently harmless antigen like pollen, food, drugs,
ARE TYPE 1 hypersensitivities (only true allergic reaction)
What is a general definition of hypersensitivity?
The immune response acting when it shouldn’t (as in to harmless antigens)
Type III? Common name, antibodies involved, how works, common sites.
Immune complex mediated diseases
IgM or IgG
Immune complexes embed in small blood vessels and trigger inflammation
Tend to be skin, kidneys, joints
Type IV? Name, time frame relative to type I? What mediates?
Name: delayed type, T cell mediated
Takes a couple days in comparison to immediate b/c it is T cell mediated
T cell mediated
ONLY ONE that is T cell mediated
If you have no antibodies/are B cell deficient; which types of hypersensitivity can you have?
Only type IV because no antibodies means no IgG, IgM, IgE, to trigger responses of types I-III
What happens during a type I reaction? (Which antibody, effects which cell, causes what reaction in body, how fast?
IgE antibodies develop against an antigen
IgE bind to mast cells
IgE cross links–>leads to mast cell degranulation
Effect: smooth muscle construction and blood vessel dilation and increase in vascular permeability
Seconds to minutes (immediate hypersensitivity)
Type 1 is also known as?
Antiparasite reaction: body thinks it is reacting to pieces of worms
Immediate hypersensitivity
Allergies
Does type 1 happen the first time body is exposed to the antibody?
No, must become sensitized to it the first time:
B cells bind,
trigger TH2 response,
TH2 tells B cell to class switch to IgE
IgE binds to Fc receptors on mast cells
Next time see: cross link receptors and trigger mast cell degranulation and the allergic response!
Cells rebuild granules and can dump them again
What type are nickel and latex allergies?
Type 4: they are not actual allergies (which is Type 1)
What is the difference between immediate and late phase reactions?
Immediate: bump, where a person was exposed to antigen, happens immediately and dies down within the hour
Late phase: increased inflammation due to mast cells retooling, other cells coming in (not everybody has this reaction), happens 4-20 hours post antigen exposure
What is lactose intolerance?
Missing an enzyme, not an allergy
Examples of type one?
Hay fever (allergic rhinitis, sinusitis)
Food allergies
Bronchial asthma
Anaphylaxis (drugs, bee sting, food): treat with epinephrine
Diagnosing allergies?
Symptomatic/seasonal symptoms
ELISA for IgE (enzyme linked immunosorgan assay)
Skin testing
What is seen for skin testing for immediate, late, and delayed reactions?
Immediate: small inflamed bump at site of antigen exposure
*15-60 minutes
Late: larger inflammation/puffiness
4-12 hours
Delayed: inflammation and puffiness 12-48 hours after initial exposure, nothing right away (Type 4)
T/F Tb skin test is always positive for vaccinated individuals
True
What is wheel and flare?
Wheel= whelts
Flare= redness around it
Diagnostic test for type 1 hypersensitivity
What happens in type 2 hypersensitivity?
Antigen binds to a cell
Triggers cell to be destroyed through complement fixation and ADCC (antibody-dependent cellular cytotoxicity)
Complement & Fc mediated inflammation
Two examples of type 2 hypersensitivity?
Transfusion reactions
Hemolytic disease of the newborn
What is a transfusion reaction?
Blood type reaction: if given wrong type you trigger cell destruction, lyse all of them (like malaria blood cells all lysing at once)
Type 2
What is hemolytic disease of the newborn?
Mother has negative blood cell type and fetus has positive
First pregnancy everything is fine, but during birth process maternal and fetal blood mix and the mother mounts an immune response against
Next positive blood child: IgG crosses placenta and mothers antibodies cross and kill fetus
Type 2
Rogam can prevent mother from mounting own antibody response
Brief review of blood group antigens
Type A has A antigen and anti-B antibodies
Type B has B antigen and anti-a antibodies
Type AB has A and B antigen and no antibodies
Type O has no antigen present and anti-A and anti-B antibodies
Graves’ disease is which type? What are some others of this type?
Type 2
Some autoimmune
Rheumatic fever: increased risk from strep not treated with antibiotics–> cross reactivity with heart antigen
Remember: this is cytotoxic: so attacks and kills own cells
What is a classic example of type 3 hypersensitivity?
Serum sickness
Bitten by snake, given antivenom (passive immunity), react to the soluble proteins from the animal the passive immunity was attained
If you get an injection and seven days later have rash, arthritis, kidney dysfunction; what is source of antibody and antigen?
If get it within the day of injection?
Human antibodies and horse antigen: seven days later immune response against serum proteins
Horse antibodies and snake venom protein: within the day
What happens in type 3 hypersensitivity?
Immune complex mediated tissue injury: circulating immune complex depsits in vascular wall, complement and Fc receptor cause recruiting and activation of inflammatory cells (neutrophils)
Vasculitis
Affects high pressure areas in circulatory system: kidneys and joints
What causes type 4 hypersensitivity?
Cell mediated immunity: T cells
Slowly developing response to antigen: peak reaction 2-3 days (instead of minutes)
Reactions can occur nearly anywhere in the body
Result from activation of sensitized T cells (memory T cells), release of cytokines, and influx of macrophages
The tuberculin skin test is a classic example of …
Type IV delayed hypersensitivity
Introduce small quantities of protein antigens from tubercle bacillus into skin
Positive: injection site reddens and gradually thickens: reaction reaches peak in 2-3 days
Negative: if never been exposed (no memory T cells)= no response
Result from activation of sensitized T cells (memory T cells), release of cytokines, and influx of macrophages
Review of what is responsible in each 1-4 hypersensitivities?
1= only IgE, activates mast cells, basophils, eosinophils
2= IgM and/or IgG, antibody binding to cell surface triggers destruction
3= IgM and/or IgG, antibody/antigen complexes bind to endothelial tissue, and triggers inflammation
4= memory T cells (only cell mediated), CD4 or CD8, triggers inflammation
What are some examples of type 4 hypersensitivity?
Type I diabetes****
Nickel, latex, poison ivy, poison oak
(Must be sensitized first time)
What is a super antigen? (Type 4 slide)
Binds outside if peptide binding groove: can activate 2-20%, can activate more T cells than standard antigen
Difference between hypersensitivity and autoimmunity?
Hypersensitivity= foreign antigen source
Autoimmunity= self antigen source
Reactions go hand in hand though, same response just different antigen sources
