[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"$fxLN3MUwXCdr5RPjwZYIDpOj8CHyjOmngWTgoKXPtZbg":3,"$f_UEhVTSgknt91cjDXd7rGlkrm-1DKCLJ8dI6oS-4uto":32,"$f3Ft0rKFJHppdzE-vuveecxx1BUcg9iOlMLtyzf_MJDg":81},[4,8,12,16,20,24,28],{"title":5,"slug":6,"path":7},"About Microbeonline.com","about-microbeonline-com","\u002Fabout-microbeonline-com\u002F",{"title":9,"slug":10,"path":11},"About Me","about-me","\u002Fabout-microbeonline-com\u002Fabout-me\u002F",{"title":13,"slug":14,"path":15},"Advertise with Us","advertise-us","\u002Fadvertise-us\u002F",{"title":17,"slug":18,"path":19},"Privacy Policy","privacy-policy","\u002Fprivacy-policy\u002F",{"title":21,"slug":22,"path":23},"Abbreviations","abbreviations","\u002Fabbreviations\u002F",{"title":25,"slug":26,"path":27},"Microbes","microbes","\u002Fmicrobes\u002F",{"title":29,"slug":30,"path":31},"Books","recommended-books","\u002Frecommended-books\u002F",{"type":33,"data":34},"blog",{"slug":35,"title":36,"description":36,"seoTitle":37,"seoDescription":37,"author":38,"createdDate":39,"lastUpdatedDate":40,"draft":41,"category":42,"image":37,"body":43,"faq":44,"tags":45,"related":47},"hypersensitivity-type-i","Hypersensitivity Type I: Mechanism and Clinical Manifestation",null,"Srijana Khanal","2022-09-21","2026-07-21",false,"immunology","Various diseases result from inappropriate and immediate immune responses to common environmental components which are otherwise not harmful. Scientists Coombs and Gell have classified such responses as hypersensitivity type I reactions. IgE antibodies are the leading cause of this reaction.\n\n**Type I hypersensitivity reaction is called immediate hypersensitivity, as an IgE response is immediate. Similarly, it is called an anaphylactic reaction (opposite of prophylaxis or protection, i.e., harmful) or allergy. The term allergy refers to the changed reactivity of the host when encountering theantigenon a second or subsequent exposure.**\n\nHypersensitivity type I is extremely common, where the release of pharmacological mediators, such as histamine, occurs by IgE-sensitized mast cells and produces an acute inflammatory response with symptoms like asthma or rhinitis. Manifestations can be local or systemic, leading to anaphylactic shock and even death.\n\n![Exposure and sensitization to allergens - Figure source:https:\u002F\u002Fmagazine.scientificmalaysian.com\u002Fissue-9-2014\u002Fallergies\u002F](https:\u002F\u002Fassets.microbeonline.com\u002Fblogs\u002Fsensatization.jpg)Figure: Figure source:https:\u002F\u002Fmagazine.scientificmalaysian.com\u002Fissue-9-2014\u002Fallergies\u002F\n\n## Components of Hypersensitivity Type I\n\n1. **Allergen**\n\nThe allergens are antigens capable of stimulating IgE production and type I hypersensitivity responses in allergic individuals on repeated exposure.\n\nForeign serum and egg albumin are potent antigens, whereas pollen is a weak antigen.\n\n**Table: Common allergens associated with hypersensitivity I (Souce: Kuby Immunology)**\n\n| Common allergen | Examples |\n| --- | --- |\n| Proteins | Foreign serum, vaccine |\n| Plant pollen | Ryegrass, ragweed, Timothy grass, birch trees |\n| Drugs | Penicillin, sulfonamides, local anesthetics, salicylates |\n| Foods | Nuts, seafood, eggs, peas, beans, milk |\n| Insect products | Bee venom, wasp venom, ant venom, cockroach calyx, dust mites |\n| Mold spores |  |\n| Animal hair and dander latex soap |  |\n\n1. **IgE**\n\nUsually, among all of the antibodies, [IgE](\u002Fimmunoglobulin-e-ige-antibodies\u002F) is secreted in the lowest amount, whereas IgE secretion rises in parasitic infection. In such cases, a high serum IgE successfully eliminates parasites. Atopy is a hereditary predisposition to developing immune hypersensitivity reaction against the common environmental antigen. This condition allows non-parasitic antigen to stimulate inappropriate IgE production, leading to tissue-damaging type I hypersensitivity. Hence, atopic patients secrete IgE 10 times more than a normal condition.\n\nOn the other hand, TH1 suppresses IgE production with the help of interferon-gamma. IgE is also called reagin since it is involved in an allergic reaction and is a cytotoxic antibody.\n\n1. **Mast cells and basophils**\n\nThe basophils are granulocytes that circulate in the blood. These are recruited into tissues at the sites of inflammation.\n\nMast cells are found throughout connective tissue, mainly near blood, lymphatic vessels, and nerves. These are also found in the respiratory and gastrointestinal tract, skin, and mucous membranes.\n\nMast cells and basophils contain pharmacologically active mediators. These mediators are released from the granules on activation, manifesting a type I hypersensitivity reaction.\n\n1. **IgE binding Fc receptor**\n\nThe reaginic activity of IgE depends on its ability to bind to a receptor specific to the Fc region of IgE. High-affinity and low-affinity receptors are present in receptor cells like mast cells and basophils.\n\n1. **Mediators and cytokines**\n\nClinical manifestations of type I reaction result from mediators released during mast cells or basophil degranulation. These mediators act on local tissues and effector cells like eosinophils, neutrophils, monocytes, T lymphocytes, and platelets. If they respond to parasitic infection, the effect is beneficial. But if allergens induce the response, this results in an unnecessary increase in vascular permeability and inflammation, which is far more detrimental than helpful.\n\nThe mediators are classified as either primary or secondary. The primary mediators are pre-made before degranulation and are stored in the granules. The secondary mediators are either synthesized after target cell activation or released by the breakdown of the cell membrane during the degranulation process. The examples of primary and secondary mediators are given in the table.\n\n## Mechanism\n\nTwo steps take place in type I hypersensitivity. The **first step is sensitization**, and the **second subsequent exposure gets serious**.\n\n**Activation of B lymphocytes to produce IgE and sensitization of mast cells**\n\nThis is the step where there is sensitization of the host and formation of IgE antibodies, which, once formed, attaches to the receptors on mast cells or basophil. This step is asymptomatic.\n\n1. **Formation of IgE**\n\nBreathe, or ingested molecule (allergen), is captured by phagocytes or antigen-presenting cells (APC) and is taken to the lymph node. APC presents allergen to T-helper cells living there. Now TH differentiates into TH2 cells. TH2 cells release interleukins (IL-4, IL-5, IL-13), switching B-cell to form plasma cells secreting IgE.\n\nAllergen induces humoral antibody response to plasma cells that produce antibodies and memory cells, as in humoral immunity. But, plasma cells secrete IgE in response to the activity of allergen-specific TH2 cells.\n\n1. **Binding of IgE to mast cells and basophils and sensitization**\n\nSensitization of mast cells and basophils requires IgE. IgE has a high affinity to the Fc receptor of the mast cell and basophil cell. Thus,**when these cells are coated with antibodies, they become sensitized.** Locally produced IgE will first sensitize the local mast cells, and the rest of the IgE enters the circulation and binds to the Fc receptors on basophils and mast cells throughout the body. The half-life of serum IgE is only 2.5 days, while mast cells may remain sensitized for up to 12 weeks.\n\n!\\[The sequence of events in hypersensitivity type I.\n\n- The sequence of events in hypersensitivity type I. Image source: Type I and Type II Hypersensitivity\\](<\u002Fsequence-of-events-544x1024.jpg)\n\n**Mast cells release chemical mediators and adversely affect the second exposure**\n\nThis is the step of reaction in response to the shocking dose. The second step includes the activation of mast cells or basophils and degranulation.\n\n1. **IgE cross-linkage and activation of mast cells and basophils**\n\nMonths later, exposure to the same allergen cross-links the membrane-bound IgE on sensitized mast cells and basophil cells. This causes degranulation following various harmful effects.\n\n1. **Degranulation of the sensitized cells**\n\nA mediator from granules damages both invading and nearby cells. This leads to vasodilation and smooth muscle contraction, causing systemic and local infection.\n\nIL5 production and activation of eosinophils and granulocytes take place in this step. It is an active process involving calcium influx, the release of primary mediators, and secondary mediators, including cytokines and chemokines. Since the patients have histamine effects, it is called histamine poisoning.\n\n**Table: Principal mediators involved in type I hypersensitivity (Source: Kuby Immunology)**\n\n| Mediators | Type | Effects |\n| --- | --- | --- |\n| Primary | Histamine, heparin | Increased vascular permeability, smooth muscle contraction |\n|  | Eosinophil and neutrophil chemotactic factors | Chemotaxis |\n|  | Protease (tryptase, chymase) | Bronchial mucus secretion, degradation of blood vessel basement membrane, generation of complement split products |\n| Secondary | Platelet-activating factor | Platelets aggregation and degranulation; contraction of pulmonary smooth muscle |\n|  | Leukotrienes | Increased vascular permeability, contraction of pulmonary smooth muscles |\n|  | Prostaglandins | Vasodilation, contraction of pulmonary smooth muscles, platelets aggregation |\n|  | Bradykinin | Increased vascular permeability, smooth muscle contraction |\n| (Secondary) Cytokines | IL – 1 and TNF | Systemic anaphylaxis, increased expression of CAMs on venular endothelial cells |\n|  | IL-4 and IL-13 | Increased IgE production |\n|  | IL-3, IL-5, IL-6, IL-10 | Various effects on innate and adaptive immunity |\n\n## Reactions of Immediate Hypersensitivity\n\nType I hypersensitivity has two presentations: an immediate reaction and a late-phase reaction.\n\n1. **Immediate Reaction**\n\nWhen a patient is exposed to an allergen, an intradermal injection of the same antigen causes redness and swelling on the injection site. This soft swelling is called a wheal, and the red rim at the margin of the wheal is a flare. This reaction occurs within 5 to 10 minutes and usually subsides in less than an hour. The cytoplasmic granules are released due to sensitization of dermal mast cells by IgE bound to the Fc receptor by cross-linking the IgE by antigen. Immediate hypersensitivity reactions include skin and mucosal allergies, food allergies, asthma, and systemic anaphylaxis.\n\n1. **Late phase reaction**\n\nIt starts in 2-8 hours and lasts 2-3 days. Wheal and flares follow 2 to 4 hours later by a late phase reaction consisting of an accumulation of inflammatory leukocytes, including neutrophils, eosinophils and basophils, and Th2 cells; or without a detectable preceding immediate hypersensitivity reaction. E.g., bronchial asthma.\n\nLate phase reaction usually is due to secondary mediators and inflammatory cell reaction. The late phase activation of mast cells and their mediators ultimately damages tissue.\n\n## Clinical manifestations\n\nThe type 1 reaction can range from the life-threatening anaphylactic reaction to milder forms associated with common allergies.\n\nImmediate hypersensitivity reactions are seen in the URT (upper respiratory tract), GIT (gastrointestinal tract), and skin. Most allergic responses occur on the mucus membrane surface when an allergen enters the body by inhalation or ingestion. Vascular and smooth muscle reaction develops after repeated exposure to the allergen (the immediate response).\n\nDiseases associated with hypersensitivity I can be described in two types: localized and systemic.\n\n1. **Localized Reaction**\n\n- Skin allergies, Hay fever, allergic rhinitis, asthma, food allergy\n- Rashes or blisters in the skin, pruritus (hives, atopic dermatitis, eczema)\n- Increased eye and nasal secretions, itching, sneezing (allergic rhinitis\u002Fhay fever, allergic conjunctivitis)\n- Oropharyngeal mucosal edema (food allergies)\n- Gastrointestinal abnormalities, like abdominal pain, diarrhea, vomiting (food allergies)\n- Bronchospasm, wheezing (bronchial asthma)\n- Urticaria and eczema\n\n1. **Systemic anaphylaxis**\n\n- Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction occurring within minutes of exposure to an allergen.\n- Large quantities of inflammatory mediators are released due to rapid systemic vasodilation, vascular permeability, hypotension, and extensive tissue edema. Fluids may be in the lungs and constrict the airways. Patients can undergo shortness of breath, lethal suffocation, cardiovascular collapse, and loss of consciousness.\n\n## Lab Diagnosis\n\n**Skin testing**\n\nHypersensitivity type I can commonly be identified and assessed by skin testing. A small amount of potential allergen is introduced at a specific skin site. Wheal and flare are seen within 30 minutes, which confirms the type I reaction.\n\n**Serum testing**\n\nSerum level of total IgE antibody can be tested based on radioimmunoassay. It can detect nanomolar levels of total IgE.\n\n## Control\n\nType I hypersensitivity can be controlled by applying the following measures:\n\n- Contact with known allergens should be avoided. Removing house pets, dust, and offending foods should be done as far as possible.\n- In severe cases, hypo sensitization or desensitization can help patients, i.e., immunotherapy with repeated injections of increasing doses of allergens, to reduce the severity or to eliminate them.\n- The use of humanized monoclonal anti-IgE can also be helpful.\n- Drug therapies, like, antihistamines, are most useful in allergic rhinitis. Glucocorticoids are also used.\n- Anaphylaxis is a medical emergency requiring immediate airway access with the administration of epinephrine and fluid resuscitation.\n\n**References**\n\n1. Kindt *et al.*(2007). Kuby Immunology. W. H. Freeman and Company. 6th edition.\n2. Abbas *et al.*(2007). Cellular and Molecular Immunology. Saunders, Elsevier. 6th edition.\n3. \u003Chttps:\u002F\u002Flabpedia.net\u002Felementary-immunology\u002Fchapter-11-type-1-hypersensitivity-reaction-anaphylaxis-atopy-and-treatment\u002F>\n4. \u003Chttps:\u002F\u002Fwww.lecturio.com\u002Fconcepts\u002Ftype-i-hypersensitivity-reaction\u002F>",[],[46],"hypersensitivity",[48,54,60,66,72],{"slug":49,"title":50,"description":50,"seoTitle":37,"seoDescription":37,"author":38,"createdDate":51,"lastUpdatedDate":40,"draft":41,"category":42,"image":37,"faq":52,"tags":53},"hypersensitivity-reactions","Hypersensitivity Reactions: an Overview","2022-11-20",[],[46],{"slug":55,"title":56,"description":56,"seoTitle":37,"seoDescription":37,"author":38,"createdDate":57,"lastUpdatedDate":40,"draft":41,"category":42,"image":37,"faq":58,"tags":59},"hypersensitivity-type-iii","Hypersensitivity Type III: Mechanisms and Clinical Manifestations","2022-10-14",[],[46],{"slug":61,"title":62,"description":62,"seoTitle":37,"seoDescription":37,"author":38,"createdDate":63,"lastUpdatedDate":40,"draft":41,"category":42,"image":37,"faq":64,"tags":65},"hypersensitivity-type-iv","Hypersensitivity Type IV: Mechanism and Clinical Manifestation","2022-10-08",[],[46],{"slug":67,"title":68,"description":68,"seoTitle":37,"seoDescription":37,"author":38,"createdDate":69,"lastUpdatedDate":40,"draft":41,"category":42,"image":37,"faq":70,"tags":71},"hypersensitivity-type-ii","Hypersensitivity Type II: Mechanism and Clinical Manifestation","2022-09-25",[],[46],{"slug":73,"title":74,"description":74,"seoTitle":37,"seoDescription":37,"author":75,"createdDate":76,"lastUpdatedDate":40,"draft":41,"category":77,"image":37,"faq":78,"tags":79},"mcq-immunology-3","MCQ Immunology (56-70): Hypersensitivity Answers with Explanations","Acharya Tankeshwar","2010-04-18","mcqs",[],[80,46],"immunology-mcqs",[82,88,95,100,104,108,113,118,121,125],{"slug":83,"name":75,"description":84,"image":85,"body":86,"postCount":87},"acharya-tankeshwar","Editor-in-chief","https:\u002F\u002Fassets.microbeonline.com\u002Fauthors\u002Ftankeshwar-acharya-author-microbeonline.jpg","***Tankeshwar Acharya, MSc (Medical Microbiology)***\n\n*Tankeshwar Acharya is an Assistant Professor in the Department of Microbiology at Patan Academy of Health Sciences (PAHS), Nepal, where he has been teaching and practicing clinical microbiology for over 14 years. He is the founder of Microbe Online, one of the leading free microbiology education resources on the web, covering bacteriology, mycology, parasitology, immunology, and clinical laboratory diagnostics written from direct experience in both the classroom and the diagnostic laboratory.*",433,{"slug":89,"name":90,"description":91,"image":92,"body":93,"postCount":94},"ashma-shrestha","Ashma Shrestha","SEO Copywriter and Science Communicator\nKathmandu, Nepal","https:\u002F\u002Fassets.microbeonline.com\u002Fauthors\u002Fashma-shrestha.png","Ashma Shrestha holds a Master of Science in Medical Microbiology from the Institute of Science and Technology (IOST), Tribhuvan University, Nepal, where she developed a strong foundation in virology, molecular biology, and diagnostic microbiology.\n\nShe now works as an SEO Copywriter at Resolution Digital, where she combines her scientific training with research-driven content strategy. She is certified in Google Analytics and Google Business Profile (GBP), and brings a data-informed approach to science communication writing content that is not only accurate but structured to reach and serve the students who need it most.\n\nAt microbeonline, Ashma contributes articles primarily in virology and molecular biology, areas she finds most compelling for their mechanistic depth and their growing clinical relevance. Her writing reflects the same standard the site is built on: factual rigor, clear explanation of the *why* behind microbiology concepts, and content that helps students move from memorization to genuine understanding.\n\nShe is passionate about making complex microbiological concepts accessible without sacrificing accuracy; a skill that sits at the intersection of her scientific training and her professional work in content and SEO.",81,{"slug":96,"name":97,"description":98,"image":37,"body":37,"postCount":99},"sushmita-baniya","Sushmita Baniya","Author \u002F Contributor",32,{"slug":101,"name":102,"description":98,"image":37,"body":37,"postCount":103},"samikshya-acharya","Samikshya Acharya",20,{"slug":105,"name":106,"description":98,"image":37,"body":37,"postCount":107},"alisha-tripathi","Alisha Tripathi",6,{"slug":109,"name":110,"description":111,"image":37,"body":37,"postCount":112},"aastha-shrestha","Aastha Shrestha"," Author \u002F Contributor",10,{"slug":114,"name":115,"description":116,"image":37,"body":37,"postCount":117},"guest-author","Guest Author","Guest Author \u002F Contributor",2,{"slug":119,"name":38,"description":98,"image":37,"body":37,"postCount":120},"srijana-khanal",18,{"slug":122,"name":123,"description":116,"image":37,"body":37,"postCount":124},"dr-poonam-acharya","Dr. Poonam Acharya",1,{"slug":126,"name":127,"description":98,"image":37,"body":128,"postCount":129},"nisha-rijal","Nisha Rijal","**Nisha Rijal** is a microbiologist and quality assurance specialist. She served for nearly 12 years as a microbiologist at the National Public Health Laboratory (NPHL), Nepal's national reference laboratory, and continues to work as a consultant microbiologist in international public health organization. ",51]