Hypersensitivity Flashcards
Major mediators of Type I hypersensitivity
IgE and Mast Cells or Eosinophils
Types of hypersensitivity reaction

Major mediators of Type II hypersensitivity
Autoreactive IgG/IgM and sometimes effector mediators of IgG (neutrophils, macrophages)
Major mediators of Type III hypersensitivity
Immune-complex-forming antibodies against soluble antigens, complement, and chronic inflammatory cells recruited to sub-endothelial immune-complex deposits.
Major mediators of Type IV hypersensitivity
CD4 and CD8 T cells and downstream effector cells driven by T-cell-derived cytokine production
Atopy
Presdisposition to developing allergies. Sometimes used synonymously with allergy.
Sensitization phase of allergy
Activation of Th2 and IL-4-secreting Tfh cells, which lead to ε heavy chain class-switching and IgE production in B cells. The IgE produced then binds to the surface of mast cells, basophils, and eosinophils via FcεRI.
Distinct phases of Type I hypersensitivity
The immediate effects are mediated by mast cell degranulation, but there is also a late-phase reaction.
This late-phase reaction happens several hours following exposure and is the characterized by infiltration of neutrophils and eosinophils in response to the mast cell signals. It is these cells which are the culprit in tissue damage associated with repeated bouts of allergic reactions.
Development of an allergy diagram

Kinetics of allergy

Genes with variants that predispose to development of allergies
IL-4
IL-4R
IL-13
IL-5
Filaggrin
Filaggrin
Protein required for barrier protection in skin. Mutations predispose to development of allergies early in life, especially atopic dermatitis.
FcεRI signaling

Principal cells involved in late-phase reaction
neutrophil
eosinophil
Th2
Late-phase reactions are stimulated by. . .
. . . IL-4 and TNF-α derived from mast cell degranulation.
Most of the actual tissue damage associated with allergy is caused by. . .
. . . eosinophil-derived proteases cleaving structural proteins.
hay fever
Allergic reaction to inhaled antigens, such as ragweed pollen antigens. This results in allergic sinusitis and rhinitis, initiated by mast cells in the nasal mucosa.
Increased mucus production and late-phase inflammation occur as a result of mast cell degranulation and Th2 activation locally.
food allergy
Ingested antigens trigger intestinal mast cell activation. Results in increased peristalsis which may cause diarrhea and vomitting.
More severe symptoms such as anaphylaxis may occur if the antigens are absorbed and become systemic.
asthma
Characterized by difficulty breathing, wheezing, coughing, and airway obstruction in response to a respiratory allergen which activates bronchial mast cells.
chronic asthma
In chronic cases of asthma, baseline eosinophilia of the airway is common, and mucus production in the airway is ramped up. Bronchial smooth muscle also hypertrophies and thus becomes hyper-reactive to various stimuli.
May be IgE-dependent or -independent, in which case cold or exercise may trigger asthma attacks.
Anaphylaxis
Systemic reaciton characterized by rapid edema in various tissues, including the larynx, and precipitous drop in blood pressure (anaphylactic shock), as well as bronchoconstriction.
A result of systemic mast cell degranulation.
Treatment for anaphylaxis
Epinephrine to contract vascular smooth muscle and relieve shock symptoms, as well as acting as a bronchodilator to counter bronchoconstriction symptoms.
Treatments for asthma
Corticosteroids, leukotriene antagonists, and β adrenergic receptor agonists.
Cromolyn
Inhibits mast cell degranulation