IMMUNE RESPONSE TO IMMEDIATE HYPERSENSITIVITY (TYPE 1)
COMPILED BY:
GROUP
1. Faza Nadhir Fadhilla (PO7134124046)
2. Rika Amelia (PO7134124059)
3. Putri Marisyah (PO7134124063)
4. Rinaldi Pratama Putra (PO7134124064) 5. Melani Mulia Putri (PO7134124082)
6. Nina Machda Lena (PO7134124083)
CLASS: 1B
ENGLISH LECTURER FIDER SAPUTRA T., S.Hum., M.Hum.
DIII TEKNOLOGI LABORATORIUM MEDIS POLTEKKES KEMENKES
PALEMBANG 2025
TABLE OF CONTENTS
_Toc193630745
TABLE OF CONTENTS... 2
A. Introduct...2
B. Immunological Mechanism of Type 1 Hypersensitivity...3
C. Chronic Phase / Late-Phase Reaction... 5
D. Clinical Manifestations of Type 1 Hypersensitivity...6
E. Diagnosis of Allergies and Type 1 Hypersensitivity...7
F. Treatment and Management of Allergies...9
CONCLUSION... 9
REFERENCES...11
VOCABULARY...11
A. . Introduct
Type 1 hypersensitivity is a rapid immune reaction triggered by allergens. This condition occurs when the immune system mistakenly identifies harmless substances as threats, leading to an exaggerated immune response. Symptoms can develop within minutes of allergen exposure, ranging from mild discomfort to life-threatening reactions.
The primary cause of Type 1 hypersensitivity is an IgE-mediated immune response.
Upon initial exposure to an allergen, the immune system produces immunoglobulin E (IgE), which binds to mast cells and basophils. When re-exposure occurs, the allergen binds to the preformed IgE, triggering the release of histamine and other inflammatory mediators. This process leads to allergic symptoms such as swelling, redness, itching, and respiratory issues.
Common examples of Type 1 hypersensitivity include food allergies, allergic rhinitis, allergic asthma, and anaphylaxis. Food allergies can cause mild skin reactions or severe swelling that affects breathing. Allergic rhinitis is characterized by sneezing, nasal congestion, and watery eyes due to exposure to pollen or dust. In allergic asthma, airway constriction results in breathing difficulties. In severe cases, anaphylaxis may occur, a medical emergency requiring immediate treatment.
4o .
B. Immunological Mechanism of Type 1 Hypersensitivity
Type 1 hypersensitivity is an exaggerated immune response mediated by
immunoglobulin E (IgE) upon exposure to specific allergens. This immune reaction is divided into two main phases: the sensitization phase (priming phase) and the effector phase (acute &
chronic reactions). The process involves multiple immune cells, cytokines, and biochemical mediators that contribute to the allergic response.
Sensitization Phase (Priming Phase)
The sensitization phase occurs during the first exposure to an allergen. At this stage, the immune system recognizes and processes the allergen, preparing for a future immune response. The steps involved in this phase include:
1. Allergen Recognition and Antigen Presentation
o When an individual is exposed to an allergen for the first time, dendritic cells (antigen-presenting cells) in the mucosal or skin tissue capture the allergen.
o The captured antigen is processed and presented on major histocompatibility complex (MHC) class II molecules to naïve CD4+ T cells, initiating an immune response.
2. Activation of T Helper 2 (Th2) Cells
o In a predisposed individual, the naïve T cells differentiate into T helper 2 (Th2) cells under the influence of specific cytokines.
o Th2 cells secrete cytokines interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13), which play a crucial role in the allergic response.
3. B Cell Activation and IgE Production
o IL-4 and IL-13 stimulate B cell differentiation into plasma cells, which are responsible for producing allergen-specific IgE antibodies.
o These IgE antibodies specifically recognize and bind to the allergen, serving as key mediators of hypersensitivity reactions.
4. Mast Cell and Basophil Sensitization
o The newly produced IgE binds to high-affinity FcεRI receptors on the surface of mast cells and basophils, effectively sensitizing these cells.
o Once sensitized, these cells remain in a primed state, ready to trigger an allergic reaction upon subsequent exposure to the same allergen.
Effector Phase (Acute & Chronic Reactions)
Upon re-exposure to the allergen, the immune system rapidly responds by activating mast cells, leading to the release of inflammatory mediators. This results in immediate allergic symptoms and, in some cases, chronic inflammation.
Subsequent Exposure → Mast Cell Activation
When the same allergen re-enters the body, it binds to the IgE antibodies that are already attached to mast cells.
This cross-linking of IgE molecules triggers mast cell degranulation, leading to the release of various mediators that contribute to allergic symptoms.
Mediators Released During Mast Cell Degranulation 1. Histamine
o Causes vasodilation, leading to redness and swelling.
o Increases vascular permeability, resulting in tissue edema.
o Triggers bronchoconstriction, leading to airway narrowing and difficulty breathing (as seen in allergic asthma).
2. Proteases (Tryptase, Kinins, and Chymase)
o Induce tissue damage by breaking down extracellular matrix proteins.
o Contribute to inflammation and increased mucus production, worsening symptoms in allergic reactions.
3. Lipid Mediators (Leukotrienes and Prostaglandins)
o Leukotrienes (LTC4, LTD4, LTE4) cause prolonged bronchoconstriction, mucus secretion, and increased vascular permeability, making them key players in asthma and anaphylaxis.
o Prostaglandins (PGD2) amplify inflammation and smooth muscle contraction, further intensifying the allergic response.
The immunological mechanism of Type 1 hypersensitivity involves a well-coordinated process between antigen-presenting cells, T helper cells, B cells, mast cells, and inflammatory mediators. The sensitization phase prepares the immune system for an allergic response, while the effector phase triggers the actual allergic symptoms upon re-exposure. Understanding this process helps in developing targeted therapies for allergic conditions, such as antihistamines, leukotriene inhibitors, and immunotherapy.
C. Chronic Phase / Late-Phase Reaction
After the initial acute allergic reaction, some individuals experience a chronic or late- phase reaction, which occurs 4–6 hours after allergen exposure. Unlike the immediate phase, which is dominated by mast cell degranulation, the late-phase reaction involves sustained inflammation due to the recruitment of additional immune cells. This phase contributes to prolonged allergic symptoms and, in severe cases, tissue remodeling and permanent damage, particularly in conditions such as chronic asthma or atopic dermatitis.
Key Features of the Late-Phase Reaction 1. Delayed Onset
o Symptoms develop hours after the initial allergic response and can persist for several days.
o Unlike the acute phase, which subsides once histamine and other mediators dissipate, the late-phase response prolongs inflammation and tissue damage.
2. Recruitment of Inflammatory Cells
o The late-phase reaction is driven by cytokine-mediated recruitment of immune cells, including:
Eosinophils → Release toxic granules (major basic protein, eosinophil cationic protein) that exacerbate inflammation and cause tissue damage.
Macrophages → Contribute to chronic inflammation by releasing pro- inflammatory cytokines.
Lymphocytes (T cells) → Secrete cytokines that sustain immune activation, promoting persistent allergic responses.
3. Increased Tissue Inflammation and Damage
o Continuous exposure to inflammatory mediators leads to chronic tissue remodeling, especially in long-term conditions like asthma and allergic dermatitis.
o Structural changes may include:
Airway thickening and fibrosis in chronic asthma, leading to irreversible airflow obstruction.
Increased mucus production, contributing to persistent breathing difficulties.
Epithelial cell damage, worsening skin and respiratory allergies.
The chronic phase of Type 1 hypersensitivity is a critical factor in the progression of allergic diseases. While the early-phase reaction is responsible for immediate symptoms, the late-phase response contributes to long-term complications. Understanding this mechanism is essential for managing chronic allergic conditions, highlighting the importance of anti-
inflammatory therapies (e.g., corticosteroids, leukotriene inhibitors, and biologics targeting eosinophils) to prevent tissue damage and disease progression.
D. Clinical Manifestations of Type 1 Hypersensitivity
Type 1 hypersensitivity reactions manifest in various clinical forms, ranging from mild allergic responses to life-threatening conditions. These reactions occur due to an IgE-
mediated immune response to allergens, leading to the release of histamine and other
inflammatory mediators. The severity of symptoms depends on the site of allergen exposure and the immune system’s response. The three major clinical manifestations include allergic rhinitis, allergic asthma, and anaphylaxis, each with distinct symptoms and physiological effects.
1. Allergic Rhinitis
Also known as hay fever, this condition is one of the most common allergic disorders.
It occurs due to inhalation of allergens, such as pollen, dust mites, or pet dander.
Symptoms include:
o Sneezing due to nasal irritation.
o Stuffy nose (nasal congestion) caused by inflammation of the nasal mucosa.
o Watery eyes and itching, resulting from histamine release affecting the conjunctiva.
2. Allergic Asthma
A chronic inflammatory condition affecting the lower respiratory tract.
Triggered by allergens like dust mites, mold, pet dander, or air pollutants.
Symptoms arise due to bronchoconstriction and airway inflammation, including:
o Shortness of breath, caused by narrowing of the airways.
o Wheezing, a high-pitched sound due to turbulent airflow.
o Increased mucus production, leading to airway obstruction and difficulty breathing.
3. Anaphylaxis (Severe Systemic Reaction)
The most severe and life-threatening form of Type 1 hypersensitivity.
It occurs due to a massive release of histamine and inflammatory mediators, often triggered by food allergies, insect stings, or medications.
Symptoms develop rapidly and can lead to shock and organ failure if untreated:
o Shock (circulatory collapse) due to widespread vasodilation.
o Hypotension (dangerously low blood pressure), reducing oxygen delivery to organs.
o Airway obstruction, caused by severe bronchoconstriction and swelling of the throat (laryngeal edema).
Understanding these clinical manifestations is essential for early diagnosis and effective management of allergic conditions. Mild cases like allergic rhinitis can be managed with antihistamines and nasal corticosteroids, whereas allergic asthma requires bronchodilators and anti-inflammatory medications. In severe cases like anaphylaxis, immediate administration of epinephrine is crucial to prevent fatal complications.
E. Diagnosis of Allergies and Type 1 Hypersensitivity
The diagnosis of allergies, including type 1 hypersensitivity, is essential for identifying specific triggers and developing effective treatment strategies. Diagnostic methods involve various tests aimed at detecting IgE-mediated immune responses to specific allergens. The three main diagnostic methods include the Skin Prick Test (SPT), serum-specific IgE test, and provocation tests, each with distinct purposes and procedures.
1. Skin Prick Test (SPT)
o A skin test used to evaluate allergic reactions to various allergens.
o Performed by applying allergen extracts to the skin and pricking the surface with a small lancet.
o If an individual is allergic to a substance, a wheal (raised bump) and flare (redness) will appear within 15–20 minutes.
o Commonly used to diagnose allergies to food, pollen, dust mites, and pet dander.
2. Serum-Specific IgE Test
o Also known as a blood test for specific IgE, measuring IgE antibody levels in the serum.
o Methods used include ImmunoCAP and ELISA.
o Helps identify specific allergens without the risk of immediate reactions as seen in SPT.
o Suitable for patients who cannot undergo skin tests, such as those with a history of anaphylaxis or severe skin conditions like dermatitis.
3. Provocation Tests
o Conducted by directly exposing the target organ to allergens, such as
inhalation for the respiratory tract, nasal mucosa, or ingestion of certain foods.
o Aimed at evaluating more complex allergic reactions under controlled conditions.
o Performed strictly under medical supervision due to the risk of severe allergic reactions, including anaphylaxis.
o Primarily used for diagnosing food or drug allergies that cannot be identified through skin or blood tests.
Allergy diagnosis must be performed carefully using appropriate methods based on the patient’s condition. The Skin Prick Test (SPT) is the primary choice for environmental allergies, while the serum-specific IgE test is recommended for individuals unable to undergo SPT. Provocation tests should only be conducted under medical supervision due to their higher risk. With accurate diagnosis, healthcare providers can develop effective treatment and prevention strategies for allergic patients.
F. Treatment and Management of Allergies
The management of allergies involves both preventive and pharmacological approaches to reduce symptoms and prevent severe allergic reactions.
1. Prevention
o Avoid exposure to known allergens such as food, dust, and pollen.
o Modify the environment to minimize allergen presence, including using air filters and controlling humidity levels.
2. Pharmacological Treatment
o Antihistamines (H1 blockers): Reduce the effects of histamine, helping alleviate symptoms like sneezing, itching, and runny nose.
o Corticosteroids: Suppress inflammation and are commonly used to treat allergic rhinitis, asthma, and skin allergies.
o Beta-agonists (e.g., Salbutamol): Help relax bronchial muscles, making them effective for treating asthma-related breathing difficulties.
o Epinephrine (Adrenaline): A life-saving emergency treatment for severe allergic reactions (anaphylaxis), helping to restore blood pressure and open airways.
o Allergen immunotherapy: A long-term treatment involving gradual
desensitization to specific allergens, reducing the severity of allergic responses over time.
By implementing these strategies, individuals with allergies can effectively manage their condition and improve their quality of life.
CONCLUSION
Type 1 hypersensitivity is a rapid allergic reaction mediated by Immunoglobulin E (IgE). This reaction occurs when the immune system overreacts to harmless substances, triggering an allergic response. The process begins with sensitization, where the body produces IgE antibodies against specific allergens. Upon subsequent exposure, these antibodies bind to mast cells, causing the release of histamine and other inflammatory mediators.
The activation of mast cells leads to inflammation, which manifests in various allergic symptoms. These symptoms can range from mild reactions, such as sneezing, itching, and hives, to severe conditions like anaphylaxis, a life-threatening emergency that requires immediate medical intervention. The severity of the response depends on the individual's sensitivity and the amount of allergen exposure.
Proper prevention and treatment are essential in managing Type 1 hypersensitivity and preventing complications. Avoiding known allergens, using medications like antihistamines and corticosteroids, and undergoing allergen immunotherapy can help control symptoms. For severe cases, carrying emergency epinephrine is crucial to prevent fatal outcomes. By taking appropriate precautions, individuals with allergies can reduce their risk and improve their quality of life.
REFERENCES
Abbas, A. K., Lichtman, A. H., & Pillai, S. (2022). Cellular and Molecular Immunology (10th ed.). Elsevier.
Murphy, K., & Weaver, C. (2016). Janeway's Immunobiology (9th ed.). Garland Science.
Parham, P. (2014). The Immune System (4th ed.). Garland Science.
VOCABULARY
Hypersensitivity (Hipersensitivitas)
→ Respons imun yang berlebihan atau tidak sesuai terhadap zat yang biasanya tidak berbahaya bagi tubuh.
Type 1 Hypersensitivity (Hipersensitivitas Tipe 1)
→ Reaksi alergi yang dimediasi oleh IgE dan terjadi dengan cepat setelah paparan alergen. Reaksi ini melibatkan pelepasan histamin dan mediator inflamasi lainnya dari mast cells dan basophils, yang menyebabkan gejala alergi seperti gatal, bengkak, dan sesak napas.
Allergen (Alergen)
→ Zat asing yang dapat memicu respons imun yang berlebihan pada individu yang sensitif, seperti serbuk sari, debu, makanan tertentu, atau bulu hewan.
Mast Cells (Sel Mast)
→ Sel imun yang mengandung granula berisi histamin dan mediator inflamasi lainnya, yang berperan dalam reaksi alergi dan inflamasi.
IgE (Immunoglobulin E)
→ Jenis antibodi yang diproduksi oleh sistem imun sebagai respons terhadap alergen. IgE berikatan dengan reseptor pada mast cells dan basophils, menyebabkan pelepasan histamin saat terjadi paparan ulang.
Histamine (Histamin)
→ Senyawa kimia yang dilepaskan oleh sel mast selama reaksi alergi, menyebabkan gejala seperti pembengkakan, gatal, dan kontraksi otot polos pada saluran napas.
Anaphylaxis (Anafilaksis)
→ Reaksi alergi sistemik yang sangat parah dan mengancam jiwa, ditandai dengan penurunan tekanan darah, kesulitan bernapas, dan pembengkakan saluran napas.
Bronchoconstriction (Bronkokonstriksi)
→ Penyempitan saluran napas akibat kontraksi otot polos di bronkus, sering terjadi pada asma alergi.
Sensitization (Sensitisasi)
→ Proses di mana sistem imun pertama kali mengenali dan bereaksi terhadap alergen dengan memproduksi IgE, menyebabkan tubuh menjadi lebih peka terhadap paparan berikutnya.
Eosinophils (Eosinofil)
→ Jenis sel darah putih yang berperan dalam reaksi alergi dan infeksi parasit, sering ditemukan dalam jumlah tinggi pada individu dengan alergi kronis.
Allergen → Alergen
Allergic reaction → Reaksi alergi Anaphylaxis → Anafilaksis Antibody → Antibodi
Antigen-presenting cell (APC) → Sel penyaji antigen Atopy → Atopi (kecenderungan genetik terhadap alergi)
Basophil → Basofil (jenis sel darah putih yang berperan dalam reaksi alergi) Bronchoconstriction → Bronkokonstriksi (penyempitan saluran napas) B cell (B lymphocyte) → Sel B (limfosit B, penghasil antibodi) Cytokines → Sitokin (protein yang mengatur respons imun)
Chemokines → Kemokin (zat yang menarik sel imun ke lokasi peradangan) Chronic inflammation → Peradangan kronis
Dendritic cells → Sel dendritik (sel penyaji antigen yang berperan dalam sistem imun adaptif) Degranulation → Degranulasi (pelepasan mediator inflamasi dari sel mast)
Eicosanoids → Eikosanoid (mediator inflamasi seperti prostaglandin dan leukotrien) Eosinophils → Eosinofil (sel darah putih yang berperan dalam reaksi alergi)
Exposure → Paparan
Fc receptor → Reseptor Fc (protein pada sel imun yang mengikat antibodi)
Food allergy → Alergi makanan
Granules → Granula (kantung kecil dalam sel mast dan basofil yang mengandung histamin) Genetic predisposition → Predisposisi genetik (faktor keturunan yang meningkatkan risiko alergi) Histamine → Histamin (senyawa yang menyebabkan gejala alergi)
Hypersensitivity reaction → Reaksi hipersensitivitas
IgE (Immunoglobulin E) → Imunoglobulin E (antibodi yang terlibat dalam alergi) Inflammation → Peradangan
Late-phase reaction → Reaksi fase lambat (inflamasi berkelanjutan setelah reaksi awal) Leukotrienes → Leukotrien (zat yang menyebabkan bronkokonstriksi dan peradangan) Lymphocytes → Limfosit (jenis sel darah putih yang berperan dalam respons imun) Mast cells → Sel mast (sel yang mengandung histamin dan berperan dalam alergi) Mediator → Mediator (zat yang mengatur proses peradangan)
Nasal congestion → Hidung tersumba
Neutrophils → Neutrofil (jenis sel darah putih yang melawan infeksi) Plasma cells → Sel plasma (sel yang memproduksi antibodi)
Prostaglandins → Prostaglandin (zat yang menyebabkan peradangan dan nyeri) Rhinitis → Rinitis (peradangan pada hidung akibat alergi)
Respiratory distress → Gangguan pernapasan
Sensitization → Sensitisasi (proses tubuh menjadi peka terhadap alergen) Shock → Syok (penurunan tekanan darah ekstrem akibat reaksi alergi) Skin prick test (SPT) → Tes tusuk kulit (uji alergi yang umum digunakan)
T helper cells (Th2 cells) → Sel T helper (Th2) (jenis limfosit T yang berperan dalam alergi) Tissue damage → Kerusakan jaringan
Tolerance → Toleransi (ketidakmampuan sistem imun untuk bereaksi terhadap alergen tertentu Vasodilation → Vasodilatasi (pelebaran pembuluh darah akibat histamin)