10- Hypersensitivity Flashcards Preview

Fundamentals Of Immunology > 10- Hypersensitivity > Flashcards

Flashcards in 10- Hypersensitivity Deck (35):

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



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



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)


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