Penicillin, sulfonamide, procaine, organic iodine compounds, etc.

Pollen particles, dust mites or their excrement, fungi or their spores, insects or their venom, animal dander or feathers, etc.

Cysteine ​​proteins, bacterial enzymes, etc. in dust mites

Milk, eggs, fish, shrimp, crab and shellfish, etc.

Produced by plasma cells in the submucosal lamina propria lymphoid tissue of the nasopharynx, tonsils, trachea, and gastrointestinal tract

Allergens activate Th2 to produce IL-4, and IL-5 → induces B cells to undergo IgE class switching and proliferate and differentiate into IgE-producing plasma cells.

Cytophilic antibodies → can bind to FcRI on the surface of mast cells/basophils through their Fc segment without binding to antigen → putting the body in a sensitized state

FcRI—high affinity receptor

FcRII—low affinity receptor

common ground

the difference

Distributed in the mucosal subepithelial tissues of the respiratory tract, digestive tract and urogenital tract

Contains eosinophilic granules that store synthesized cationic proteins, major basic proteins, neurotoxins, peroxidase, and collagenase

preformed medium within particles

Newly synthesized medium after activation

Allergen exposure occurs within seconds

lasts for hours

Caused by histamine, prostaglandins

Telangiectasis, increased vascular permeability, smooth muscle contraction, and increased glandular secretion

Mast cells release large amounts of cytokines to promote eosinophil activation

4-6 hours of exposure to allergen

lasts for several days

Inflammatory response dominated by infiltration of granulocytes, macrophages, and Th2 cells

Penicillin is the most common, followed by aspirin and non-steroidal anti-inflammatory drugs

Clinical serum preparations: tetanus antitoxin, diphtheria antitoxin, etc.

Respiratory allergic reactions caused by inhalation of allergens such as pollen, dust mites, fungi, animal dander, etc.

Nausea, vomiting, abdominal pain, diarrhea and other symptoms caused by ingested allergens

Those prone to food allergies are deficient in slgA and proteolytic enzymes in the gastrointestinal tract

Includes urticaria, atopic dermatitis (eczema), and angioedema

Caused by drugs, food, intestinal parasites, or other irritants

Contactless

Detailed medical history (exposure history, allergy history)

Allergen testing

Skin test: penicillin, antitoxin, pollen extract, etc.

Small amounts and multiple injections at short intervals (antitoxin)

Pollen, dust mites, etc.

Inhibits mediator synthesis-aspirin

Inhibitory mediator release – disodium cromoglycate, epinephrine

Diphenhydramine, chlorpheniramine, acetyl salicylic acid, etc.

Adrenaline raises blood pressure

Calcium gluconate, calcium chloride, vitamin C relieve spasms

Inhibits mast cells and basophils

Inhibit IL5 activity and treat eosinophilic syndrome

Promote Th2 type immunity to Th1 type

Normally existing allotype antigens (ABC blood group antigens, RH antigens, HLA antigens)

heterophile antigen

Autoantigens changed by infection or physical and chemical factors

Foreign antigen or hapten adsorbed to cells

Antibody

cell

complement

After IgM or IgG binds to target cell surface antigens, it activates the classical complement pathway and kills target cells.

Activation of phagocytosis through Fc receptors or complement receptors on the surface of phagocytes

The IgG antibody binds to target cells, and its Fc segment binds to the Fc receptor on NK cells to mediate cell killing.

Red blood cells—drug-induced hemolytic anemia

Granulocytosis - granulocytopenia

Platelets—thrombocytopenic purpura

include

mechanism

antigen

symptom

mechanism

symptom

mechanism

symptom

Mediates inflammatory damage

Cytotoxicity

Secrete inflammatory factors and cause chronic inflammation

Contact dermatitis can occur in some individuals when exposed to paints, dyes, cosmetics, pesticides, drugs, or certain chemicals