HypersensitivityHypersensitivity – Exaggerated immune response that have deleterious effects and causes damage to the individual.
Anaphylaxis – an immediate hypersensitivity reaction triggered by mast cell degranulation. Can be local or systemic.
Prophylaxis - measures designed to preserve health and prevent the spread of disease; protective or preventive treatment.
Can be: immediate or delayed (DTH)
HypersensitivityClassification based on immune response:
Type I – IgE-Mediated
Type II – Antibody-Mediated Cytotoxic
Type III – Immune Complex-Mediated
Type IV – Delayed-Type (DTH)
HypersensitivityType I – IgE-Mediated Hypersensitivity
cross-linking of IgE to mast cells and basophils results in systemic and local anaphylaxis
Type I – IgE-mediated Hypersensitivity
Type I – IgE-mediated HypersensitivityAllergens – antigens that induce type I hypersensitivity
Type I – IgE-mediated Hypersensitivity
IgE cross-linkage initiates degranulation
Type I – IgE-mediated Hypersensitivity
Mediators of Type I Reactions:
Primary HistamineSerotoninChemotactic factorsProteases
SecondaryPlatelet-activating factorLeukotrienesProstaglandinsBradykininCytokines
systemic anaphylaxislocal anaphylaxis
Allergic rhinitisAsthmaFood allergiesAtopic dermatitis
Treatment of Type I hypersensitivity
AntihistaminesCromolyn sodiumTheophyllineEpinephrineCortisone
Type I – IgE-mediated Hypersensitivity
HypersensitivityType II – Antibody-Mediated Cytotoxic Hypersensitivity
Antibodies mediate destruction via complement or ADCC
Type II HypersensitivityType II – Antibody-Mediated Cytotoxic Hypersensitivity
Type II Hypersensitivity
HypersensitivityType III – Immune Complex-Mediated Hypersensitivity
Antibody-antigen complexes activate complement
Immune Complex-Mediated Hypersensitivity
Type III Hypersensitivity
HypersensitivityType IV – Cell-Mediated Hypersensitivity
Cytokine release activate macrophages and TC cells
Type IV - Hypersensitivity
Type IV - Hypersensitivity
Type IV - Hypersensitivity
Type IV Hypersensitivity