Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

11 Cards in this Set

  • Front
  • Back
Components of an allergic response
standard Ig structure
Mast cells and Basophils
both express high affiinity FcER
both contain histamine, TNF-a, and leukotrienes in cytoplasm
Mast cell- tissue bound, compartmentalized as mucosal or conn tissue, contain potent vasoactive compounds
Mast cells contain large amt of histamine, proteases, leukotriene B4 (LTG4), heparin and inflammatory cell cytokines that include IL 3, 4, 5, 6, 8, TNF-a, chemokines and GM-CSF.
When these cells release these very potent mediators, important conseq ensue
There is a direct relationship btwn serum IgE levls, allergic rxn and the atopic state.
Genetic background
any allergen- almost anything can be an allergen but there is a trend towards proteins with enzymatic activity or ones that induce it.
Timing is important: decreased early exposure to infections in genetically predisposed indivudiual is associated with insuffiicient T regulator control of IgE
route- mucosal exposure predominated
Describe the sequence of the allergic response
First exposure to antigen- usually mucosal (resp or GI) but can be cutaneous or systemic
extraction of antigen-by antigen presenting cells (DC) via "allergic" TLR that induces the DC to produce IL-4 instead of IL-12
presentation of the allergen as immunodominant peptide in a Class II MHC groove.
Allergic reponses depend on Th2 activiation.
Th2 cells prived the critical IL-4 signal to an allergen specific B cell
accelerated prod of TH2 ctyokines espec IL3 and IL13 dominate
Promotion of IgE calls switinch occurs upreglation of CD-23 on mast cells adn basophils that increase IL4 and IL 13
iL 4 from TH2, Basophils and mast cells active E germ line trx in B cells and results in IgE synthesis
What is the Late Phase Response
Late phase response is secondary to the release of mediators of cells that were recruited to the site of massive degranulation.

Is completely dependent on T-cell activiation and presence of cytokines IL3, 4, 5,13, TNF-a, GM-CSF, and IL10
IL3, 5, GM-CSF amplify eosinophil production by bone marrow
Characterized by eosinophils
What are the clinical manifestations of an allergic response
strongly dependent on the site of the reaction
anaphylaxis with laryngeal and brochiolar constriction and generalized increase in vascular.
They can be fatal.

Allergic rhinitis
Hives (urticaria) - skin lesions occur when IgE armed mast cells are activated in skin
Acute and chronic bronchial asthma occurs when IgE armed cells are recruited to submucosal sites of the pulmonary bronchi
see fig 10.18
genetic predisposition
environmental condition (right allergen at right time, small fam = hygiene hypothesis, etc.)
T reg cell deficiency
Triggers lead to IgE antibodies
leads to allergic syndromes
Why is there are marked increase in asthma in the industrial world
Hygiene Hypothesis
decr. childhood infection and later exposure
early exposure to less see page 10
Allergen in solid phase
IgE ()serum
IgE binds to allergen
radiolabeled anti-IgE

only used in children of people who can't do the skin test