Hypersensitivity & Autoimmunity (gaily trans)

• What is the definition of hypersensitivity?

  Exaggerated response to a typically harmless antigen that results in injury to the tissue, disease, or even death.
• What are the types of hypersensitivity and their classifications?

  • Type I, II, III: Immediate hypersensitivity (symptoms develop within minutes to hours)
  • Type IV: Delayed hypersensitivity (manifestations seen after 24 to 48 hours)
• What is Type I hypersensitivity also known as?

  Anaphylactic hypersensitivity.
• What mediates Type I hypersensitivity?

  It is mediated by antibodies, primarily IgE.
• What is a distinguishing feature of Type I hypersensitivity?

  There is a short time lag, with symptoms usually exhibiting within minutes after exposure to the allergen.
• What are allergens?

  Antigens that trigger Type I hypersensitivity.
• Give examples of common allergens.

  Peanuts, eggs, pollens, seafood.
• What does atopy refer to?

  Inherited tendency to respond to inhaled and ingested allergens with continued production of IgE.
• What is the origin of the term "atopy"?

  Derived from the Greek word “Atopos” meaning out of place.
• How does the immune response differ in individuals with allergies?

  The immune response is shifted, with TH2 cells predominating, leading to the production of cytokines like IL-4 and IL-13.
• What are the key immunologic components in Type I hypersensitivity?

  IgE, mast cells, basophils, and eosinophils.
• What role does histamine play in Type I hypersensitivity?

  Histamine is a mediator that causes different allergic reactions.
• What are the two major phases of Type I hypersensitivity?

  1. Sensitization Phase:

  • IgE attaches to FcεRI receptors.
  • B cells produce allergen-specific IgE.

  1. Activation Phase:

  • Mast cells bind allergen-specific IgE.
  • Degranulation occurs, releasing mediators like histamine.
• What happens during the sensitization phase of Type I hypersensitivity?

  The IgE antibody attaches to high affinity receptors called FcεRI, and B cells produce allergen-specific IgE.
• What occurs during the activation phase of Type I hypersensitivity?

  Mast cells bind allergen-specific IgE and undergo degranulation, releasing mediators like histamine.
• What is anaphylaxis?

  A severe form of allergy.
• What are secondary mediators in Type I hypersensitivity?

  Secondary mediators are more potent than primary mediators and are responsible for late phase allergic reactions.
• What are the clinical manifestations of Type I hypersensitivity?

  They depend on antigen exposure, dose, and frequency, leading to symptoms like asthma or rhinitis.
• What happens if the allergen is ingested?

  It may result in gastrointestinal symptoms and can trigger systemic responses.
• What are common clinical examples of Type I hypersensitivity?

  • Rhinitis: sneezing, rhinorrhea, runny nose.
  • Asthma: breathlessness caused by inhalation of small particles.
  • Food allergies: common reactions to ingested allergens.
  • Dermatitis: includes urticaria or hives.
• What are the treatment options for Type I hypersensitivity?

  • Avoidance: first line of defense.
  • Medications: anti-histamines, bronchodilators, corticosteroids.
  • Epinephrine: for systemic anaphylaxis.
  • Anti-IgE monoclonal antibody (Omalizumab): prevents IgE binding.
  • Allergy Immunotherapy (AIT): induces immune tolerance.
• What are the testing methods for Type I hypersensitivity?

  • In Vivo Skin Tests: Percutaneous and Intradermal tests.
  • Allergen-Specific IgE Testing: Radioallergosorbent Test (RAST).
  • In Vitro Tests: Radio Immunosorbent Assay (RIST).
• What is Type II hypersensitivity also known as?

  Mediated cytotoxic hypersensitivity.
• What antibodies are involved in Type II hypersensitivity?

  IgG and IgM antibodies directed against antigens on cell surfaces.
• What are the major effects of Type II hypersensitivity?

  • Cellular destruction.
  • Inhibition of cell function.
  • Increased cell function above normal.
• What are clinical examples of Type II hypersensitivity?

  • Transfusion Reactions: acute and delayed hemolytic reactions.
  • Hemolytic Disease of the Newborn: maternal IgG destroys fetal red blood cells.
  • Autoimmune Hemolytic Anemia: formation of antibodies against one's own cells.
• What is the cause of acute hemolytic transfusion reactions?

  IgM involvement associated with the ABO blood group, occurring within minutes or hours after incompatible blood transfusion.
• What are the symptoms of acute hemolytic transfusion reactions?

  Symptoms include DIC, vascular collapse, renal failure, fever, chills, nausea, lower back pain, tachycardia, shock, and hemoglobin in urine.
• What characterizes delayed hemolytic reactions?

  IgG involvement occurring within the first two weeks following a transfusion due to anamnestic response.
• What is the treatment for hemolytic disease of the newborn?

  Anti-D immune globulin (Rhogam) is administered at 28 weeks of gestation and within 72 hours after delivery.
• What is the difference between warm and cold autoimmune hemolytic anemia?

  Warm autoimmune hemolytic anemia is characterized by IgG antibodies reacting at 37°C, while cold autoimmune hemolytic anemia involves IgM reacting best at cold temperatures.
• What are the testing methods for Type II hypersensitivity?

  • Direct Antiglobulin Test (DAT): detects transfusion reactions and hemolytic disease.
  • Indirect Coomb’s Test: used in crossmatching to prevent transfusion reactions.
• What is Type III hypersensitivity also known as?

  Complex-mediated hypersensitivity.
• How does Type III hypersensitivity differ from Type II?

  Type III involves soluble antigens and destruction is complement mediated, while Type II involves cell surface antigens.
• What are clinical examples of Type III hypersensitivity?

  • Arthus Reaction: local immune complex deposition causing necrotic dermal reaction.
  • Serum Sickness: results from passive immunization with animal serum.
• Who demonstrated the Arthus Reaction?

  Maurice Arthus.
• What occurs during the Arthus Reaction?

  Localized inflammatory reaction occurs with erythema and edema, peaking at 3 to 8 hours after antigen injection.
• What is serum sickness associated with?

  Passive immunization of humans with animal serum, historically using horse antiserum.
• What is Type IV hypersensitivity also known as?

  Cell-mediated hypersensitivity.
• What is the mechanism of Type IV hypersensitivity?

  • Involves T cells rather than antibodies.
  • Delayed response to antigen exposure.
  • Can lead to tissue damage.