Flashcards in Type I Immunopathology and Parasite Immunity Deck (49):
What is the true role of IgE and Th2?
Is IgG produced in a person infected with worms?
Yes. and it activates complement and recruits neutrophils
Are neutrophils able to kill helminths?
No they lack a helminthocidal mechanism
When a mast cell binds antigens to it FcR the mast cell degranulates what does it release?
What does histamine do to the smooth muscle of the gut?
Increases contraction and violent peristalsis
What do the prostaglandins and leukotrienes do (released as ECF=A2)?
Attract eosinophils in large numbers
Eosinophils have Fc receptors that recognize IgG. How does that help it recognize the worm it needs to kill?
Because IgG is already opsonizing the worm at this point
What do the eosinophils do after the Fc receptor binds the IgG + helminth?
It releases the content of its granules Including Major Basic Protein which is highly toxic the the helminth
What is the role of Th2-like Tfh cells?
They go to the lymph node and help B cells switch to IgE production
What is the role of Th2 cells in helminth infection?
They go to the site of infection and attract both eosinophils and macrophages
What do Th2 cells produce to recruit eosinophils and macrophages?
What do IL-4, IL-5, and IL-13 do to macrophages?
Activate them to the alternative M2 pathway where they heal damage and wall off M1-resistant invaders
Eosinophilia in the blood is indicative of what?
1. Parastie infection
2. Type II immunopathology
What are allergens?
Antigens that cause allergy
When will a mast cell degranulate?
When two adjacent IgE molecules are bound to the same antigen
What does histamine do the the bronchial smooth muscle?
Is it common to see a type I immunopathology reaction to an antigen that can penetrate intact skin?
What is allergic rhinitis?
Seasonal (August and September) allergy to ragweed
Causes runny nose and itchy eyes
What is eczema?
Chronic dry and easily irritated skin, itch, and rash caused by an allergen
Secondary bacterial infections are common
What is oral allergy syndrome?
Almost immediate allergy to foods that causes tingling lips and tongue, itching, and swelling of the lips
ONLY oral cause stomach acid causes degradation of allergen
Asthma is considered both __________ and _________.
broncoconstrictive and inflammatory
It is important to avoid fibrosis
What is hyper IgE syndrome?
Autosomal Dominant condition
Inability to make INF gamma
So Th2 dominant
High IgE, skin abscesses and fungal and Pseudomonas pneuonia
What percentage of people experience allergic symptoms at some time in their life?
A newborn with two parents who have allergies has a _____% of developing allergies.
Is the incidence of asthma on the rise or decline?
Give an example of a cross-reaction.
Cantaloupes cross-react with ragweed; people with ragweed rhinitis can have cantalouope oral allergy syndrome
What is atopic state?
Prone to develop any of the range of allergic syndroms
Infant with eczema can go on to have allergies to fish or milk, or develop asthma
Production of IgE is dependent upon what?
IgE binds to that two cells that have Fc(epsilon)RI?
Basophils (found in blood)
Mast cells (found in tissue)
SUPER HIGH BINDING AFFINITY
What does degranulation release?
What clinical symptoms does histamine produce?
Blood vessel dilation
What occurs in the late phase reaction?
Phospholipase PLA2 cleaves arachidonic acid from membrane phospholipids
Converted into prostaglandins by COX and leukotrienes by lipoxygenase
What is the role of prostaglandins and leukotrienes?
They initiate inflammation, constrict bronchioles, and are together called "eosinophil chemotactic factor of anaphylaxis"
What are the two phases of Type I reactions?
Describe immediate phase
Due to histamine, so can be blocked by antihistamines
Antihistamines are receptor antagonists
Describe late phase
Onset: 4-10 hours
Dependent on prostaglandins, leukotrienes, and cytokines
Eosinophils are attracted to ECF-A and IL-4 what are these mediators produced by?
ECF-A is produced by Mast cells
IL-4 is produced by Th2
Name some things that can trigger bronchospasms in hyperreactive lungs.
Irritants in the air
What is chronic spontaneous urticaria CSU?
IgG antibody against the Fc(epsilon)R1 on mast cells >>>>Chronic stimulation of histamine release
Tx: mAb omalizumab (binds to Fc or IgE so it can't bind to mast cells)
What is the most important diagnostic tool for diagnosing allergy?
Does a positive skin test conclusively mean that the patient is allergic to that allergen?
No. Cross-reactivity could be occuring
ImmunoCAP-FEIA is used to diagnose a specific allergen, but is it safe?
Yes. CAP testing is completely safe, unlike skin test which have some risk
What is asthma?
Reversible bronchoconstricitive disease with progressive inflammation leading to fibrosis
How is asthma diagnosed?
Spirometry-measures air flow
Measure FEV1- volume of air that can be forcibly exhaled from full lungs in 1 second
Then you measure FEV1 again once they get a bronchodilator treatment
Th2 in the lungs is proinflammatory. Why is this bad? How can you treat it?
Inflammation leads to fibrosis which is irreversible
Antihistamines are effective for what phase of a type I reaction?
How does epinephrine help treat anaphylaxis?
Constricts blood vessels, but dilates bronchial smooth muscle
What is the role of the following in the treatment of type I reactions:
-LABAs (Lone-Acting Beta-2 Agonists)
-Glucocorticoids: Local anti-inflammatory. Systemic has a lot of side effects. Block PG and LT synthesis and cause apoptosis in eosinophils
-Leukotriene Inhibitors: Block either synthesis (Zileuton) or binding (Montelukast)
-Rescue Inhaler: Short-acting beta-2 antagonist
-LABAs: reduce bronchoconstriction (Fluticasone/salmeterol
-IgE blocker: Omalizumab
Immunotherapy: Dilute solution of allergen extracts mechanism not clear. Oral desensitization. Peanut allergen skin patch