18. Type 1 hypersensitivity Immediate hypersensitivity. Type I - anaph

18. Type 1 hypersensitivity Immediate hypersensitivity. Type I - anaphylactic Type 1 hypersensitivity - here the antigen is always foreign and free, the antibody is always IgE , which is fixed on mast cells. (example: pollen (antigen) is foreign to the body and at the same time in the outside world it is free, once in the respiratory tract, humoral immunity is activated, which produces IgE against pollen, ultimately this immunoglobulin is fixed on mast cells) + cannot circulate in the bloodstream Once an antigen reaches, for example, the bronchi, it activates a macrophage, which in turn phagocytizes it. By phagocytizing, they expose class 2 molecules to the MHC complex. The antigen is phagocytosed by type 2 t-helper cells. T-helper type 2 has a T-cell receptor ( TCR ) and a C D -4 positive cell. CD -4 binds to the MHC molecule, and the TCR to the antigen. T-helper type 2 activates its genome (as it happens, the mitosis gene is activated) the t-helper begins monoclonal reproduction (with mono, all these resulting t- helpers are configured against the antigen), it also activates 2 genes that are responsible for the synthesis of interlekin-4 (IL-4) and interlekin-5 (IL-5). Also nearby are B-lymphocytes, which have B-cell receptors on their surface and they also have an antigen on their surface. They are in very small quantities and in order for them to multiply they need t-helper and produces IL-4, thereby stimulating its mitosis, they multiply. Then again the t-helper gives IL-5 and the resulting b-lymphocytes turn into a plasma cell, which then turns into an antibody. These plasma cells are capable of synthesizing IgE class. This immunoglobulin cannot exist in free form and immediately binds to the mast cell. A mast cell has an antibody on which there are a number of areas: 1. The site that binds to the antigen ( F a b - antigen binding site) 2. Fc fragment it can specifically land on a mast cell This immunoglobulin E lands on the mast cell with an Fc fragment and the mast cell is immediately activated and migrates to the affected area. And thus she sits there and waits for such a reaction again. Those. this IgE will be specific against this pollen. And once again, this finger immediately sits on this IgE located on the mast cell and degranulation of the mast cell occurs. It degranulates and releases all its inflammatory mediators, which will locally damage this area. Localize this antigen so that it does not cause systemic inflammation. Inflammatory mediators are divided into primary and secondary. Primary:  Histamine  Serotonin  Eosinophil chemotaxis factor (ECF)  Neutrophil chemotaxis factor (NCF) Secondary:  Tumor necrosis factor (TNF)  Interleukin-1 (IL-1)  IL-3  IL-4  IL-5  IL-6 The difference between primary and secondary is that they are already ready - they are located in the mast cell. Secondary ones require activation of the mast cell genome. During degranulation, the mast cell immediately produces primary mediators. FCE and FCN these two factors are called eosinophils and neutrophils, meanwhile histamine will dilate the vessels so that more cells come in and the permeability of the vessel increases (there are endothelial cells in the vessel that contract, thereby the endothelial pores increase, therefore, more fluid enters and occurs swelling) and spasmogenic effect (smooth myocytes have receptors for histamine, histamine acts on smooth myocytes and they contract). All this leads to shortness of breath in the patient. The lumen of the bronchi swells, narrows, and will stimulate the secretion of the glands (there will be a lot of mucus in the lumen). In addition to histamine, there will also be serotonin and secondary inflammatory mediators. The secondary ones will have a similar effect.  IL-3 and IL-5 are strong chemotactic factors of eosinophils and neutrophils. Secondary mediators are synthesized through genome activation. The genome is activated and secondary mediators are synthesized. Both IL-3 and IL-5 immediately call eosinophils and neutrophils, which begin to destroy everything, destroy blood vessels. The platelet activator is activated. The metabolite of archidonic acid is also activated on the mast cell membrane. Archidonic acid can undergo two activation pathways:  Lipoxygenase produces leukotrienes  Cytooxygenase produces prostaglandins Which are all vasodilators Ultimately, the mast cell wants to achieve 4 things:  Vasodilation  Increased permeability  Spasmogenic effect  Increased mucus secretion Examples: 1. Allergic rhinitis 2. Allergic conjunctivitis 3. hay fever 4. Anaphylactic shock: The patient is allergic to a certain drug, he already has antibodies to that drug, he already has mast cells with IgE around the vessels. And if the patient is injected with that drug, then in all the blood vessels around which mast cells are located, they are activated and begin to release these inflammatory mediators in large quantities, which lead to these 4 effects. Severe vascular collapse occurs. Diagnostics: prick test (the allergen is injected intradermally/supercutaneously and we observe the reaction; if there are already mast cells, then there will be a reaction); Rust test (radio allergy sorbent test: we can determine the IgE class against a specific antigen; specific antigens will be added). Explain it like in a presentable manner its too complex

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18. Type 1 hypersensitivity Immediate hypersensitivity. Type I - anaphylactic Type 1 hypersensitivity - here the antigen is always foreign and free, the antibody is always IgE , which is fixed on mast cells. (example: pollen (antigen) is foreign to the body and at the same time in the outside world it is free, once in the respiratory tract, humoral immunity is activated, which produces IgE against pollen, ultimately this immunoglobulin is fixed on mast cells) + cannot circulate in the bloodstream Once an antigen reaches, for example, the bronchi, it activates a macrophage, which in turn phagocytizes it. By phagocytizing, they expose class 2 molecules to the MHC complex. The antigen is phagocytosed by type 2 t-helper cells. T-helper type 2 has a T-cell receptor ( TCR ) and a C D -4 positive cell. CD -4 binds to the MHC molecule, and the TCR to the antigen. T-helper type 2 activates its genome (as it happens, the mitosis gene is activated) the t-helper begins monoclonal reproduction (with mono, all these resulting t- helpers are configured against the antigen), it also activates 2 genes that are responsible for the synthesis of interlekin-4 (IL-4) and interlekin-5 (IL-5). Also nearby are B-lymphocytes, which have B-cell receptors on their surface and they also have an antigen on their surface. They are in very small quantities and in order for them to multiply they need t-helper and produces IL-4, thereby stimulating its mitosis, they multiply. Then again the t-helper gives IL-5 and the resulting b-lymphocytes turn into a plasma cell, which then turns into an antibody. These plasma cells are capable of synthesizing IgE class. This immunoglobulin cannot exist in free form and immediately binds to the mast cell. A mast cell has an antibody on which there are a number of areas: 1. The site that binds to the antigen ( F a b - antigen binding site) 2. Fc fragment it can specifically land on a mast cell This immunoglobulin E lands on the mast cell with an Fc fragment and the mast cell is immediately activated and migrates to the affected area. And thus she sits there and waits for such a reaction again. Those. this IgE will be specific against this pollen. And once again, this finger immediately sits on this IgE located on the mast cell and degranulation of the mast cell occurs. It degranulates and releases all its inflammatory mediators, which will locally damage this area. Localize this antigen so that it does not cause systemic inflammation. Inflammatory mediators are divided into primary and secondary. Primary:  Histamine  Serotonin  Eosinophil chemotaxis factor (ECF)  Neutrophil chemotaxis factor (NCF) Secondary:  Tumor necrosis factor (TNF)  Interleukin-1 (IL-1)  IL-3  IL-4  IL-5  IL-6 The difference between primary and secondary is that they are already ready - they are located in the mast cell. Secondary ones require activation of the mast cell genome. During degranulation, the mast cell immediately produces primary mediators. FCE and FCN these two factors are called eosinophils and neutrophils, meanwhile histamine will dilate the vessels so that more cells come in and the permeability of the vessel increases (there are endothelial cells in the vessel that contract, thereby the endothelial pores increase, therefore, more fluid enters and occurs swelling) and spasmogenic effect (smooth myocytes have receptors for histamine, histamine acts on smooth myocytes and they contract). All this leads to shortness of breath in the patient. The lumen of the bronchi swells, narrows, and will stimulate the secretion of the glands (there will be a lot of mucus in the lumen). In addition to histamine, there will also be serotonin and secondary inflammatory mediators. The secondary ones will have a similar effect.  IL-3 and IL-5 are strong chemotactic factors of eosinophils and neutrophils. Secondary mediators are synthesized through genome activation. The genome is activated and secondary mediators are synthesized. Both IL-3 and IL-5 immediately call eosinophils and neutrophils, which begin to destroy everything, destroy blood vessels. The platelet activator is activated. The metabolite of archidonic acid is also activated on the mast cell membrane. Archidonic acid can undergo two activation pathways:  Lipoxygenase produces leukotrienes  Cytooxygenase produces prostaglandins Which are all vasodilators Ultimately, the mast cell wants to achieve 4 things:  Vasodilation  Increased permeability  Spasmogenic effect  Increased mucus secretion Examples: 1. Allergic rhinitis 2. Allergic conjunctivitis 3. hay fever 4. Anaphylactic shock: The patient is allergic to a certain drug, he already has antibodies to that drug, he already has mast cells with IgE around the vessels. And if the patient is injected with that drug, then in all the blood vessels around which mast cells are located, they are activated and begin to release these inflammatory mediators in large quantities, which lead to these 4 effects. Severe vascular collapse occurs. Diagnostics: prick test (the allergen is injected intradermally/supercutaneously and we observe the reaction; if there are already mast cells, then there will be a reaction); Rust test (radio allergy sorbent test: we can determine the IgE class against a specific antigen; specific antigens will be added). Explain it like in a presentable manner its too complex

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Rewrite Type I hypersensitivity as concise exam notes

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