Understanding Allergens and Type I Hypersensitivity

SCENARIO 3 Itchy A 20 year old student complained of an itchy nose, watery eyes and sneezing after cleaning his boarding room. Symptoms are accompanied by bumps all over the body. This is often felt every time you inhale dust. It is known that this reaction occurs due to the release of chemical mediators by certain immune cells due to an excessive response. After taking certain medications, the symptoms felt decrease. Explain the types of antigens as allergens Tutor Instruction Questions LO 1: 1. What can be classified as an allergen? The adaptive immune system is an important body defense in fighting microbial infections. An immune response that is too sensitive to an antigen can cause a reaction called hypersensitivity. This response is sometimes difficult to control, attacks the host's tissue, or is triggered by commensal microorganisms or antigens from the environment. Antigens that can induce hypersensitivity reactions are calledallergen. Most allergens are proteins from the environment, animal products, and chemicals that can modify body proteins. Examples of allergens are proteins in pollen (pollen), mites, animal dander, food, chemicals such as antibiotics (penicillin). Two important characteristics of allergens are repeated exposure and generally do not stimulate innate immune responses associated with macrophage and T cell dendritic cell secretion.H1 and T-inducing cytokinesH17. Repeated cell activation in the absence of strong innate immunity can drive CD4+ T cells specifically toward the T pathwayH2. There are no specific structural characteristics of proteins that can predict whether they will be allergenic. Several characteristics exist, including low to medium molecular weight (5 to 70 kD), stability, glycosylation, and high solubility in body fluids. Some nonprotein substances, such as the antibiotic penicillin, can elicit a strong IgE response. These drugs react chemically with amino acid residues in body proteins to form haptencarrier conjugates, which induce IL-4 production from T cell responses.Hand IgE production. Repeated antigen exposure is an important determinant of the amount of specific IgE antibodies produced. Repeated exposure to a particular antigen is necessary for the development of an allergic reaction to the antigen due to a change to the IgE isotype and sensitizationmast cells with IgE must occur before a rapid-type Explain the mechanism of type I hypersensitivity reactions LO 2 Tutor Instruction Questions: 1. How does a type 1 hypersensitivity reaction occur? Rapid type hypersensitivity or type I hypersensitivity occurs due to reactions that occur due to the release of mediators from mast cells, and depends on immunoglobulin E (IgE) antibodies against environmental antigens. This hypersensitivity reaction also occurs due to activation of IL-4, IL-5, and IL-13 produced by Th2. The sequence of events in the occurrence of a type 1 hypersensitivity reaction includes: activation of Th2 cells and secretion of IL-4 by follicular helper T cells (Tfh), which stimulates the production of IgE antibodies in response to antigen; IgE binding to IgE-specific Fc receptors on mast cells; upon subsequent exposure to antigen, cross-linking of IgE binds to the antigen, leading to mast cell activation and release of various mediators. Some mediators released by mast cells cause a rapid increase in vascular permeability and smooth muscle contraction, resulting in many symptoms. Other mast cell mediators are cytokines that recruit neutrophils and eosinophils to the reaction site over several hours. There are 2 processes that occur in type 1 hypersensitivity reactions: i. Activation of Th2 cells and production of IgE antibodies Upon exposure to allergens, IL-4 secreted by Tfh stimulates the change in B lymphocyte cells to become plasma cells that secrete IgE. In atopic individuals, excessive IgE production occurs. IL-4 and IL-13 secreted by Th2 cells induce several allergic responses and reactions such as intestinal motility and excessive mucus secretion. Th2 cells also secrete IL-5 which causes eosinophilic inflammation. Production of IL-5 and IL-4 by T cells can occur in atopic individuals or have certain genes that code for cytokines or receptors involved in B lymphocyte and T lymphocyte cell responses. ii. Mast cell activation and mediator secretion IgE antibodies produced in response to allergens bind to high affinity Fc receptors specific for the ε heavy chain expressed on the surface of mast cells. In atopic individuals, mast cells are coated with IgE (sensitization) so that mast cells become sensitive to activation by antigen. Activation of mast cells due to allergen binding to more than 2 IgE antibodieson cells. MoleculeFcεRI carrying IgE is cross-linked, which triggers the signalon FcεRI resulting in the release of inflammatory mediators. Important mediators are produced by mast cells are vasoactive amines and proteases, arachidonic acid, and cytokines. This mediatorhave different actions. The amine group, namely histamine, causes an increasevascular permeability and vasodilation, thereby causing the release of plasma proteinstowards surrounding tissue, and stimulation of bronchial and intestinal smooth muscle contact.Protease can cause damage to surrounding tissue. Arachidonic acid metabolitesincluding prostaglandins causing vascular dilation and leukotrienes causingprolonged contraction of bronchial smooth muscles. Cytokines cause local inflammation.Mast cell mediators are responsible for acute vascular and smooth muscle reactionsand prolonged inflammation. Cytokines produced by mast cells stimulate recruitmentleukocytes that cause late phase reactions. The leukocytes that play a role in this condition areeosinophils, neutrophils, and Th2 cells. TNF stimulates mast cells, and IL-4 causesInflammation is dominated by neutrophils and eosinophils. Neutrophils and eosinophilsreleases proteases that cause tissue damage and Th2 makes things worseby producing many cytokines. Eosinophils are dominant in many allergic reactions andis an important cause of tissue injury. These cells are activated by the cytokine IL-5produced by Th2 cells and innate lymphoid cells.