• Occurs after a person expose to an antigen

• The body of the person responds to an antigen by producing a specific type of antibody Ig E.

• Different components that can trigger Type 1 Hypersensitivity:

Food products, such as nuts, shellfish, and soy

Animal sources, such as cats, rats, or bee stings

Environmental sources, such as mold, latex, and dust

Allergic conditions (allergic rhinitis, allergic asthma, and conjunctivitis)

Type 2 Hypersensitivity

• Occurs after a person expose to an antigen

• The body of the person responds to an antigen by producing a specific type of antibody Ig G but also involve in Ig M.

• Causes cytotoxic reactions which lead to long terms damage to cells and tissues.

Type 3 Hypersensitivity

• Antigens and antibodies form complexes in the skin, blood vessels, joints, and kidney tissues.

• Cause a series of reactions that lead to tissue damage.

• Causes of a type 3 hypersensitivity reaction can include:

Drugs that contain proteins from different organisms (antivenins)

Drug infliximab, use to manage autoimmune conditions

Animal sources (insect stings or tick bites)

Type 4 Hypersensitivity

• Reactions are cell-mediated.

• Instead of antibodies, T cells control type 4 hypersensitivity reactions.

Common causes of Type 4 Hypersensitivity include:

Exposure to poison ivy

Certain metals

drugs (antibiotics or anticonvulsants)

• Allergic rhinitis: Sneezing, runny nose, nasal congestion, itchy eyes.

• Asthma: Wheezing, shortness of breath, chest tightness.

• Anaphylaxis: Rapid onset of difficulty breathing, swelling (especially of the face, lips, and throat), drop in blood pressure, hives, nausea, vomiting.

  
  

Type II Hypersensitivity (Cytotoxic)

• Hemolytic anemia: Fatigue, pallor, shortness of breath, dark urine (due to hemoglobinuria), jaundice.

• Goodpasture's syndrome: Hemoptysis (coughing up blood), difficulty breathing, blood in urine, kidney failure.

• Myasthenia gravis: Muscle weakness, drooping eyelids, difficulty swallowing, difficulty breathing.

  
  

Type III Hypersensitivity (Immune Complex-Mediated)

• Systemic lupus erythematosus (SLE): Butterfly-shaped rash on the face, joint pain, fatigue, kidney problems, photosensitivity.

• Post-streptococcal glomerulonephritis: Blood in urine, swelling (edema), high blood pressure, kidney dysfunction.

• Serum sickness: Fever, rash, joint pain, lymphadenopathy (swollen lymph nodes).

  
  

Type IV Hypersensitivity (Delayed-Type)

• Contact dermatitis: Red, itchy rash, blisters, swelling at the site of contact with an allergen (e.g., poison ivy, nickel).

• Tuberculin reaction: Red, indurated (hardened) skin at the injection site of the tuberculin test.

• Chronic transplant rejection: Gradual loss of organ function (e.g., increased blood pressure, reduced urine output in kidney transplant rejection), organ-specific symptoms.

• IgE antibodies: Produced by B cells in the response to the allergen. Binds to the Fc receptors on mast cells and basophils.

• Mast cells and Basophils: Contains granules filled with histamine and other inflammatory mediators that are released upon activation by allergen-bound IgE antibody.

• Histamine: Released by mast cells and basophils. Causes vasodilation, increased vascular permeability, and bronchoconstriction.

Type II Hypersensitivity (Cytotoxic)

• IgG and IgM antibodies: Directed against specific antigens present on cell surfaces.

• Complement system (Classical pathway): Activated by the binding of IgG and IgM on cell surfaces. Involved in the recruitment of inflammatory cells and leads to the formation of Membrane Attack Complexes (MAC) which causes cell lysis.

• Macrophage and Neutrophils: Effector cells. Macrophages can be activated by antibodies bound to target cells and contribute to phagocytosis and tissue damage. Neutrophils are recruited by the complement system and contributes to tissue damage through the release of Reactive Oxygen Species (ROS) and proteolytic enzymes.

Type III Hypersensitivity (Immune-Complex Mediated)

• IgG and IgM antibodies: IgG is the primary antibody involved in forming immune complexes but IgM can also be sometimes involved in immune complex formation. The antibodies bind to soluble antigens to form immune complexes.

• Immune complexes (Antigen-Antibody complex): Forms when IgG or IgM binds to soluble antigens.

• Macrophage and Neutrophils: Recruitment of these cells at the the places where the immune complexes are deposited. Causes inflammation reactions and tissue destruction.

Type IV Hypersensitivity (Delayed-Type)

• CD4+ T Helper Cells (Th1) and CD8+ Cytotoxic T cells: T Lymphocytes. CD4+ T Helper Cells recognize antigens presented by Antigen-Presenting Cells (APCs) and release cytokines that help recruit and activate immune cells. CD8+ Cytotoxic T cells directly kill cells presenting the antigen.

• Dendritic cells: Antigen-Presenting Cell (APC) that captures and presents antigens to T cells, initiating an immune response.

• Macrophages: Activated macrophages releases inflammatory mediators, phagocytoses pathogens, and can act as an Antigen-Presenting Cell (APC).

• Adrenaline, or epinephrine, which is used in emergency situations to counteract anaphylaxis by relaxing muscles in the airways and tightening blood vessels.

• Systemic glucocorticoids, which reduces inflammation and suppress immune response.

• Antihistamines, which blocks histamine receptors to reduce symptoms.

Type II Hypersensitivity:

• Systemic glucocorticoids, which reduces inflammation and suppress immune response.

• Cyclophosphamide and cyclosporin agents, which inhibits the immune response to prevent damage to target cells.

• Intravenous immunoglobulin infusions, which administering pooled immunoglobulins to moderate the immune response.

• Plasmapheresis, which helps removing circulating antibodies from the blood.

• SLE

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Used for joint pain and pleurisy.

Corticosteroids: Low doses such as prednisone for inflammation.

Immunosuppressive Agents: Medications like cyclophosphamide and mycophenolate are used, especially in cases of lupus nephritis.

Antimalarials: Hydroxychloroquine is often prescribed to manage skin and joint symptoms.

Biologics: Belimumab is a biologic drug that can help reduce disease activity

• Post-Streptococcal Glomerulonephritis

Antibiotics: To eliminate any remaining streptococcal bacteria.

Diuretics: To reduce swelling (edema) by removing excess fluid from the body.

Antihypertensives: To manage high blood pressure.

Corticosteroids: In severe cases, to reduce inflammation.

• Serum Sickness

Antihistamines: To manage allergic symptoms.

Corticosteroids: To reduce severe inflammation.

Analgesics: For pain relief.

Plasmapheresis: In severe cases, to remove immune complexes from the blood.

Type IV hypersensitivity (Delayed)

• Contact Dermatitis

Topical Steroids: To reduce inflammation and itching.

Emollients: To moisturize and protect the skin.

Avoidance: Identifying and avoiding the allergen is crucial.

• Tuberculin Reaction

Topical Steroids: To reduce inflammation.

Antihistamines: For itching and discomfort.

• Chronic Transplant Rejection

Immunosuppressive Drugs: Such as tacrolimus, cyclosporine, and mycophenolate.

Corticosteroids: To reduce inflammation.

Regular Monitoring: To detect early signs of rejection and adjust treatment accordingly.

Ref for type 4:

https://www.ncbi.nlm.nih.gov/books/NBK562228/