1. What type of antibody is involved in Type I hypersensitivity and to what receptors on the mast cell or basophil does it bind?

IgE

The thick end of the epsilonRI

2. What mediators are involved in the Type I primary inflammatory response (i.e., early phase) and where do they originate in the mast cell?

-Stored in the granules and are histamines, TNF-alpha, cheomokines

-They originate in the granules

3. Name the secondary mediators of the Type I response and how are they formed?

Prostoglandins, thromoxanes, and leukotrienes, and proteins(cytokines)

4. Why is it postulated that atopic allergy has a genetic component. How do atopic persons react to common environmental substances (ie., what is produced by their immune system) that is not seen in non-atopic persons?

-Because if both of your parents have it, you are twice as likely to have it.  If neither parent has it, you are half as likely to have it.

-The atopic person will produce IgE antibodies against allergen.

5. Describe a positive result when allergy testing using the prick or scratch test.

Prick/scratch: Wheel and flare response: the bigger the falre, the more allergic they are. Skin becomes red and raised and appear itchy.

RAST: The suspected allergen is bound to an insoluble material and the patient’s serum is added.  If the serum contains antibodies to the allergens, those antibodies will bind to the allergen.

6. Is there a common property of antigens (allergens) that stimulate an IgE response in atopic persons?

7. Differentiate between localized Type I anaphylaxis and systemic anaphylaxis in terms of life threatening manisfestations.

Localized Type 1 anaphylaxis: Hay fever, atopic not contact dermatitis, brochoconstriction, hives

System Anaphylaxis: Can cause death quickly. Drop in blood pressure, throat constriction, vomiting, cramps, brochoconstriction.

8. Using drug induced type II hypersensitivity, differentiate Type I and Type II hypersensitivity when considering mode of action (i.e., mast cells, complement system)

Type 1: IgE antibodies and involved mast cells

Type 2: IgG and IgM and activates the compliment system

9. What are three examples of Type II hypersensitivity? What role do haptens play?

Transfusion blood reactions, Rh-Maternal-fetal incompatibility, drug induced

Heptin identifies the RBC as an antigen and the immune system identifies it as a foreign cell.

10. What commonality does Type I and Type III hypersensitivity have?

They involve mast cells and basophils

11. In Type III hypersensitivity, what part of the Ab-Ag complex fits into the receptor on the mast cell? What is the name of this receptor? What types of cells are attracted to the area once the mast cells are activated? How are these cells activated?

-The thick end.

-Thick gamma R3 receptor

-they attract neutrophils

-They are stimulated by the Fc end of the IgG antibodies releasing inflammatory factors that cause tissue destruction.

12. Historically, what were the most common causes of serum sickness? Why?

-The antitoxins that were given

-b/c the antitoxin wasn’t clean.  The antibodies were made by the horse and were found to be incompatible.

13. The term “serum sickness” is presently used to describe syndromes that occur after what medical events?

lupus erythematosus.

14. Symptoms of “serum sickness” are very similar to a type I systemic allergic reaction. What is the differences between these two reactions in terms of onset of symptoms?

The clinical picture doesn’t present until 10-14 days following the antigen introduction as opposed to minutes to hours in Type 1.

15. Using Farmer’s Lung disease, explain the Arthus reaction in terms of why the reaction occurs at the site of introduction.

With Farmer’s Lung, they get it by breathing in dust containing spores of peacial, heat-tolerating bacteria or molds found in moldy crops.  First there is a primary response where the person begins to produce antibodies.  But constant inhalation with stimulate secondary responses and eventually a high concentration of antibodies against specific bacteria or molds will develop.  Eventually, the antige3n will react with the antibodies at the site of introduction (Not systemic) which would be the lungs, causing type 3 reaction resulting in alveolitis.

16. What characteristic separates Type IV hypersensitivity from the other three? What specific T cell is activated and how does this cell illicit the response? Give three examples of Type IV hypersensitivity, and include the term intracellular agent.

All types involve humoral production of antibodies, where type 4 is a cytotoxic response.

TH1 helper T cells

Atpic dermatitis, latex allergen, tuberculosis

17. Why is the term delay-type hypersensitivity (DTH) used to describe type IV hypersensitivity.

It’s a delayed response, days later. This was called delayed long before they understood the type three which is actually longer.

18. What two cells are involved in the sensitization phase of type IV hypersensitivity? Which of these cells is stimulated into differentiation and clonal expansion?

Antigen presenting macrophages, TH1 cells

TH1 cell

19. What two cells are involved in the effector phase of type IV hypersensitivity and how do they interact?

TH1 clones activate the macrophages and this causes the inflammation

20. Define immunologic tolerance/immunologic homeostasis. When and how does it develop?

Develops in humans during the embryonic period-eliminates all lymphocytes that react to self HLA Class 1 and Class II antigens

-Autoreactive lymphocytes are either not iliminated or ir bit suppressed

-Recognize self-antigens as foreign.

-Involves both humoral and cytotoxic

-Can be specific to a group of cells.

---Genetically linked to the presence of specific class 1 or class 2 MHC alleles.

Mimicry: Ankylosis spondilytis: The pathogen will acticvate the immune system which will produce antibodies which suppress the oathogen.  Certain HLA alleles are better at presenting pathogen peptides which resemble self peptides to T cells.

Explain the negative selection model using HLA DR3 and DR4 alleles.

Failure of negative selection: Certain HLA alleles are less efficient at presenting self peptides to developing t calles in the thymus.  For ex: Type 1 diabetes: strongly linked to the presence of HLA DR3 and DR4 alleles.  People with these antigens have a higher risk of developing diabetes.