Podcast
Questions and Answers
Which of the following is NOT a mechanism of Type II hypersensitivity?
Which of the following is NOT a mechanism of Type II hypersensitivity?
- Antibody-induced cellular dysfunction
- Antibody-mediated opsonization and phagocytosis
- Complement activation and inflammation
- Direct cytotoxic killing by antibody-dependent cell-mediated cytotoxicity (ADCC) (correct)
Which of the following is a characteristic of the late phase of a Type I hypersensitivity reaction?
Which of the following is a characteristic of the late phase of a Type I hypersensitivity reaction?
- Rapid onset with symptoms typically resolving within 30 minutes
- Dominant involvement of mast cells and basophils
- Release of preformed mediators like histamine and neutral proteases
- Recruitment of inflammatory cells such as eosinophils, neutrophils, and Th2 cells (correct)
Which of the following diseases is NOT an example of Type II hypersensitivity?
Which of the following diseases is NOT an example of Type II hypersensitivity?
- Myasthenia gravis (correct)
- Autoimmune hemolytic anemia
- Goodpasture's syndrome
- Pemphigus vulgaris
In the context of Type II hypersensitivity, antibodies directed against exogenous antigens can arise from:
In the context of Type II hypersensitivity, antibodies directed against exogenous antigens can arise from:
Which of the following is NOT an example of antibody-induced cellular dysfunction in Type II hypersensitivity?
Which of the following is NOT an example of antibody-induced cellular dysfunction in Type II hypersensitivity?
Which of the following statements regarding the treatment of Type II hypersensitivity is TRUE?
Which of the following statements regarding the treatment of Type II hypersensitivity is TRUE?
In the context of Type II hypersensitivity, what is the primary role of the complement system?
In the context of Type II hypersensitivity, what is the primary role of the complement system?
Which of the following is a key difference between Type I and Type II hypersensitivity?
Which of the following is a key difference between Type I and Type II hypersensitivity?
Which of the following is NOT a key feature of the mechanism of negative selection in the thymus?
Which of the following is NOT a key feature of the mechanism of negative selection in the thymus?
What is the primary outcome of receptor editing in B cells?
What is the primary outcome of receptor editing in B cells?
What is the role of the transcription factor FOXP3 in regulatory T cells?
What is the role of the transcription factor FOXP3 in regulatory T cells?
Which of the following is NOT a suppressive action of regulatory T cells?
Which of the following is NOT a suppressive action of regulatory T cells?
Which of the following scenarios would most likely lead to autoimmunity?
Which of the following scenarios would most likely lead to autoimmunity?
What is the primary function of regulatory T cells in the context of immune tolerance?
What is the primary function of regulatory T cells in the context of immune tolerance?
How does the secretion of IL-10 by regulatory T cells contribute to immune tolerance?
How does the secretion of IL-10 by regulatory T cells contribute to immune tolerance?
Which of the following is a key difference between negative selection in the thymus and the suppressive action of regulatory T cells?
Which of the following is a key difference between negative selection in the thymus and the suppressive action of regulatory T cells?
Which of the following is NOT a mechanism by which Treg cells directly suppress effector T cell activation?
Which of the following is NOT a mechanism by which Treg cells directly suppress effector T cell activation?
Which of the following checkpoint receptors, when blocked, can potentially enhance anti-tumor immunity?
Which of the following checkpoint receptors, when blocked, can potentially enhance anti-tumor immunity?
Which of the following statements ACCURATELY describes the role of IL-10 in immune regulation?
Which of the following statements ACCURATELY describes the role of IL-10 in immune regulation?
Which of the following is a key difference between CTLA-4 and PD-1?
Which of the following is a key difference between CTLA-4 and PD-1?
How does FcgRIIB contribute to immune regulation?
How does FcgRIIB contribute to immune regulation?
Which of the following is NOT a potential therapeutic implication of enhancing Treg activity?
Which of the following is NOT a potential therapeutic implication of enhancing Treg activity?
Which of the following mechanisms of Treg suppression relies on the depletion of an essential amino acid for T cell proliferation?
Which of the following mechanisms of Treg suppression relies on the depletion of an essential amino acid for T cell proliferation?
What is a potential consequence of a dysfunctional or insufficient number of Tregs?
What is a potential consequence of a dysfunctional or insufficient number of Tregs?
What laboratory finding is indicative of glomerular damage in Goodpasture's Syndrome?
What laboratory finding is indicative of glomerular damage in Goodpasture's Syndrome?
Which of these is NOT a typical feature of Rapidly Progressive Glomerulonephritis (RPGN) in Goodpasture's Syndrome?
Which of these is NOT a typical feature of Rapidly Progressive Glomerulonephritis (RPGN) in Goodpasture's Syndrome?
The presence of anti-GBM antibodies is a specific marker for what condition?
The presence of anti-GBM antibodies is a specific marker for what condition?
What imaging finding is suggestive of alveolar hemorrhage in Goodpasture's Syndrome?
What imaging finding is suggestive of alveolar hemorrhage in Goodpasture's Syndrome?
Which treatment aims to remove circulating anti-GBM antibodies in Goodpasture's Syndrome?
Which treatment aims to remove circulating anti-GBM antibodies in Goodpasture's Syndrome?
What is the role of cytotoxic drugs like Cyclophosphamide in the treatment of Goodpasture's Syndrome?
What is the role of cytotoxic drugs like Cyclophosphamide in the treatment of Goodpasture's Syndrome?
Why is it essential to have both lung and renal involvement for a diagnosis of Goodpasture's Syndrome?
Why is it essential to have both lung and renal involvement for a diagnosis of Goodpasture's Syndrome?
Which of these is a supportive care strategy for respiratory symptoms in Goodpasture's Syndrome?
Which of these is a supportive care strategy for respiratory symptoms in Goodpasture's Syndrome?
Which of these is NOT a component of the basement membrane targeted by antibodies in Goodpasture's Syndrome?
Which of these is NOT a component of the basement membrane targeted by antibodies in Goodpasture's Syndrome?
What is the most common class of immunoglobulin involved in Goodpasture's Syndrome?
What is the most common class of immunoglobulin involved in Goodpasture's Syndrome?
What is the main mechanism responsible for tissue damage in Goodpasture's Syndrome?
What is the main mechanism responsible for tissue damage in Goodpasture's Syndrome?
Besides antibodies against the basement membrane, what other type of antibody can contribute to the inflammatory response in Goodpasture's Syndrome?
Besides antibodies against the basement membrane, what other type of antibody can contribute to the inflammatory response in Goodpasture's Syndrome?
Which of these HLA alleles is associated with an increased risk of developing Goodpasture's Syndrome?
Which of these HLA alleles is associated with an increased risk of developing Goodpasture's Syndrome?
Which of the following is NOT a typical symptom of Goodpasture's Syndrome?
Which of the following is NOT a typical symptom of Goodpasture's Syndrome?
Which of these statements about the prevalence of Goodpasture's Syndrome is incorrect?
Which of these statements about the prevalence of Goodpasture's Syndrome is incorrect?
What is the significance of the Goodpasture's Syndrome case originally described by Ernest Goodpasture in 1919?
What is the significance of the Goodpasture's Syndrome case originally described by Ernest Goodpasture in 1919?
Why are hypersensitivity diseases difficult to treat, according to the text?
Why are hypersensitivity diseases difficult to treat, according to the text?
What is the main issue in hypersensitivity reactions that causes tissue damage?
What is the main issue in hypersensitivity reactions that causes tissue damage?
Which of the following is NOT a cause of hypersensitivity reactions?
Which of the following is NOT a cause of hypersensitivity reactions?
What is the role of effector T lymphocytes in hypersensitivity reactions?
What is the role of effector T lymphocytes in hypersensitivity reactions?
What is the difference between an allergy and an autoimmune reaction?
What is the difference between an allergy and an autoimmune reaction?
What is the most accurate description of the 'self-tolerance' principle in the context of the immune system?
What is the most accurate description of the 'self-tolerance' principle in the context of the immune system?
What is the primary reason why hypersensitivity diseases are often described as chronic?
What is the primary reason why hypersensitivity diseases are often described as chronic?
What is the main consequence of excessive responses to microbial antigens or their prolonged presence in the body?
What is the main consequence of excessive responses to microbial antigens or their prolonged presence in the body?
Flashcards
Hypersensitivity
Hypersensitivity
A group of immune reactions causing tissue damage instead of protection.
Autoimmunization
Autoimmunization
Immune reactions against self-antigens due to loss of self-tolerance.
Self-tolerance
Self-tolerance
The immune system's ability to tolerate self-antigens without attacking them.
Environmental antigens
Environmental antigens
Harmless substances that can cause allergic reactions in some individuals.
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Cross-reactions
Cross-reactions
When antibodies mistakenly react with both microorganisms and host tissue.
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Tissue damage mechanisms
Tissue damage mechanisms
Methods like antibodies and effector T cells that damage tissues instead of pathogens.
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Chronic hypersensitivity reactions
Chronic hypersensitivity reactions
Persistent immune reactions that are hard to control and treat.
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Causes of hypersensitivity
Causes of hypersensitivity
Triggers including self-antigens, persistent microbes, and environmental allergens.
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IgE Cross-Linking
IgE Cross-Linking
Allergen binding to IgE on mast cells triggering degranulation.
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Mast Cell Degranulation
Mast Cell Degranulation
Release of preformed mediators like histamine from mast cells.
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Histamine Effects
Histamine Effects
Causes vasodilation, increased permeability, and mucus secretion.
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Late Phase Reaction
Late Phase Reaction
Develops 4-6 hours after immediate reaction; lasts 12-24 hours.
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Cytokine Recruitment
Cytokine Recruitment
Inflammatory cells are recruited by cytokines like TNF and IL-5.
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Type II Hypersensitivity
Type II Hypersensitivity
Caused by antibodies against surface antigens on cells or tissues.
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Opsonization
Opsonization
IgG/IgM antibodies mark cells for destruction by phagocytosis.
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Antibody-Induced Dysfunction
Antibody-Induced Dysfunction
Antibodies block or activate cellular functions, as seen in Myasthenia gravis.
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Goodpasture's Syndrome
Goodpasture's Syndrome
A systemic vasculitis caused by antibodies against basement membranes in renal glomeruli and pulmonary alveoli.
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Epidemiology
Epidemiology
Occurs in 1-2 cases per million yearly, mainly in young white males under 40.
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Anti-basement Membrane Antibodies
Anti-basement Membrane Antibodies
Autoantibodies targeting type IV collagen in the basement membrane, particularly in the lungs and kidneys.
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Complement System Activation
Complement System Activation
Binding of antibodies leads to complement activation, forming the membrane attack complex (MAC).
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Symptoms of Goodpasture's
Symptoms of Goodpasture's
Systemic symptoms include flu-like signs; pulmonary symptoms include cough, dyspnea, hemoptysis.
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Genetic Predisposition
Genetic Predisposition
Association with MHC alleles like HLA-DRB1*1501 increases risk of autoimmune response.
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ANCA Antibodies Role
ANCA Antibodies Role
Anti-neutrophil cytoplasmic antibodies may worsen tissue damage in Goodpasture's patients.
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Alveolar Hemorrhage
Alveolar Hemorrhage
Bleeding in the lungs leading to symptoms like cough and bloody sputum.
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Rapidly Progressive Glomerulonephritis (RPGN)
Rapidly Progressive Glomerulonephritis (RPGN)
A nephritic syndrome marked by proteinuria, hematuria, oliguria, hypertension, and potential for renal failure.
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Elevated ESR
Elevated ESR
Increased erythrocyte sedimentation rate indicating inflammation in the body.
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Hematuria
Hematuria
The presence of red blood cells in urine, indicating potential kidney damage.
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Direct Contact Suppression
Direct Contact Suppression
Tregs reduce effector T cell activation via inhibitory molecules.
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Role of Tregs in Autoimmunity
Role of Tregs in Autoimmunity
Tregs prevent autoimmunity by suppressing self-reactive lymphocytes.
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Crescent Formation
Crescent Formation
A histopathological finding in RPGN, indicating severe glomerular damage.
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Plasmapheresis
Plasmapheresis
A treatment to remove anti-GBM antibodies and inflammatory mediators from blood.
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PD-1 Function
PD-1 Function
PD-1 suppresses T cell activity by binding to PD-L1/PD-L2.
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Hypochromic Anemia
Hypochromic Anemia
Low hemoglobin levels often due to chronic blood loss or hemorrhage, seen in Goodpasture's.
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CTLA-4 Mechanism
CTLA-4 Mechanism
CTLA-4 competes with CD28 for binding, inhibiting T cell activation.
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IL-10 Role
IL-10 Role
IL-10 suppresses pro-inflammatory cytokines and APC function.
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Anti-GBM Antibodies
Anti-GBM Antibodies
Specific antibodies found in Goodpasture’s syndrome, attacking kidney and lung tissues.
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TGF-β Effects
TGF-β Effects
TGF-β inhibits T cell functions and promotes Treg differentiation.
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FcgRIIB Function
FcgRIIB Function
FcgRIIB inhibits B cell activation through immune complexes.
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IDO Role in Immune Suppression
IDO Role in Immune Suppression
IDO depletes tryptophan, leading to T cell suppression.
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Tolerance
Tolerance
The immune system's ability to avoid reacting to self-antigens.
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Mechanisms of Tolerance
Mechanisms of Tolerance
Processes that eliminate or suppress self-reactive lymphocytes to prevent autoimmunity.
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Negative Selection
Negative Selection
The elimination of high-affinity self-reactive lymphocytes during development.
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AIRE Protein
AIRE Protein
Facilitates expression of self-antigens in the thymus for T cell selection.
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Regulatory T Cells (Tregs)
Regulatory T Cells (Tregs)
Subgroup of CD4+ T cells that suppress immune responses and maintain tolerance.
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FOXP3
FOXP3
A transcription factor critical for Treg development and function.
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IL-10
IL-10
A cytokine secreted by Tregs that inhibits pro-inflammatory responses.
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Receptor Editing
Receptor Editing
The process by which autoreactive B cells rearrange their immunoglobulin genes.
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Immune System Diseases
- Immune reactions are typically protective but can cause tissue damage.
- Hypersensitivity is a group of immune reactions that lead to tissue damage due to excessive or improperly directed immune system responses.
- The immune system operates on a balance to eliminate pathogens without harming tissues.
- Sometimes immune responses become uncontrolled or target harmless antigens or the body's own tissues.
- Autoimmunization is a reaction against self-antigens (failure of self-tolerance) resulting in an attack on the body's own cells and tissues.
- Reactions to microorganisms occur when excessive immune responses to microbial antigens or prolonged exposure leads to tissue damage (e.g., tuberculosis, post-streptococcal glomerulonephritis).
- Cross-reactions arise when antibodies react with both microorganisms and host tissue (e.g., rheumatic fever).
- Environmental antigens like pollen, animal dander, dust, or metals trigger allergic reactions.
- Drug allergies are reactions to substances harmless to most people.
- In hypersensitivity, tissues are damaged by mechanisms normally used to fight pathogens like antibodies, effector T lymphocytes, and cells such as macrophages and eosinophils.
Mechanisms of Tissue Damage
- Mechanisms of tissue damage include antibody responses, effector T lymphocytes, and cells like macrophages and eosinophils, which normally combat pathogens.
- The key issue is the inappropriate activation and persistence of immune responses.
Why Are Hypersensitivity Diseases Difficult to Treat?
- It's difficult to eliminate triggers, such as self-antigens (autoimmunization), persistent microorganisms (e.g., Mycobacterium tuberculosis), and environmental antigens (allergens).
- The immune system has self-reinforcing mechanisms, which complicate controlling the chronic hypersensitivity reactions.
Hypersensitivity Reaction Summary
- Hypersensitivity refers to abnormal immune responses causing tissue damage instead of protection.
- The cause can be reactions to self-antigens, microorganisms, or allergens.
- These are chronic diseases, and difficulty eliminating triggers poses therapeutic challenges.
Classification of Hypersensitivity Reactions
- Hypersensitivity reactions are categorized into four types based on the immune mechanisms causing damage.
- Three types involve antibodies, while one is mediated by T lymphocytes.
Type I - Immediate Hypersensitivity (Allergy)
- Mechanism: Th2 cells, IgE, mast cells, and other leukocytes.
- Process: IgE binds to mast cells; mast cells release mediators acting on blood vessels and smooth muscles; cytokines recruit inflammatory cells.
- Examples: Asthma and allergic rhinitis.
Type II - Antibody-Mediated Disorders
- Mechanism: IgG and IgM antibodies bind to antigens on cells or within tissues.
- Process: Antibodies promote phagocytosis or cell lysis; inflammation and disruption of cellular functions occur without cell destruction.
- Examples: Hemolytic disease of the newborn and pemphigus.
Type III - Immune Complex-Mediated Disorders
- Mechanism: Immune complexes (antigen-antibody) deposit in tissues, causing inflammation.
- Process: Antigen-antibody complexes form in blood or tissues, activating complement and recruiting inflammatory cells.
- Inflammation causes tissue damage.
- Examples: Systemic lupus erythematosus (SLE) and post-streptococcal glomerulonephritis.
Type IV - T Cell-Mediated Hypersensitivity
- Mechanism: Mediated by CD4+ helper T cells (Th1 and Th17) and CD8+ cytotoxic T lymphocytes (CTLs).
- Process: CD4+ T cells recognize antigens presented by APCs, release cytokines for macrophage activation and inflammation; CD8+ T cells directly kill target cells expressing antigens.
- Tissue damage is from prolonged inflammation or direct cytotoxicity.
- Examples: Contact dermatitis, type 1 diabetes, and tuberculosis (granuloma formation).
Type I Hypersensitivity (Immediate)
- A rapid tissue reaction (usually within minutes) caused by an antigen coming into contact with IgE on mast cells.
- The antigen (allergen) triggers the allergic reaction.
- Examples: Hay fever, asthma, and anaphylaxis.
Course of Type I Hypersensitivity Reaction
- Th2 cells produce IL-4, IL-5, and IL-13, inducing class switching in B cells to produce IgE.
- IL-5 activates eosinophils.
- Mast cells express FcɛRI receptors for IgE to respond to allergens.
- Allergens binding to IgE triggers degranulation and release of inflammatory mediators.
Mediators in Type I Hypersensitivity Reaction
- Vasoactive amines (e.g., histamine) cause vasodilation, increased vascular permeability, smooth muscle contraction, and mucus secretion.
- Neutral proteases damage tissue and produce kinins.
- Newly synthesized lipid mediators (e.g., prostaglandin D2, leukotrienes LTC4, LTD4, and LTB4) increase mucus secretion, cause bronchoconstriction, and recruit neutrophils and eosinophils.
- Cytokines (e.g., TNF and chemokines) recruit leukocytes during the late phase.
Development of Allergy and Genetic Predispositions
- Atopy is a genetic predisposition to allergic reactions, characterized by higher levels of IgE and Th2 cells.
- 50% of individuals with atopy have a positive family history.
- Genes associated with predispositions include HLA, cytokine-related genes, FcɛRI, and ADAM33.
- Environmental factors like pollution, infections, and lack of exposure to microorganisms (hygiene hypothesis) may influence allergy development.
Phases of Type I Hypersensitivity Reaction (Sensitization and Immediate Phases)
- Sensitization Phase: Initial exposure to an allergen, antigen-presenting cells (APCs) presenting the allergen to naive T cells, T cell differentiation into Th2 cells, Th2 cell cytokine production stimulating B cells to produce allergen-specific IgE, and IgE binding to FcεRI receptors on mast cells/basophils.
- Immediate Phase (Effector Phase): Re-exposure to the allergen, allergen cross-linking IgE on mast cells triggering degranulation and release of preformed mediators (e.g., histamine, neutral proteases).
- Newly synthesized lipid mediators (e.g., prostaglandins and leukotrienes) amplify the response, causing bronchoconstriction and inflammation.
Examples and Clinical Symptoms of Type I Hypersensitivity
- Allergic Rhinitis (Hay Fever): Pollen, sneezing, nasal congestion, itchy eyes.
- Asthma: Allergens, bronchoconstriction, wheezing, shortness of breath, coughing.
- Food Allergies: Peanuts, shellfish, milk, etc., nausea, vomiting, abdominal cramps, hives, anaphylaxis.
- Atopic Dermatitis (Eczema): Environmental allergens or irritants, itchy, inflamed, dry skin.
- Anaphylaxis (Severe Systemic Reaction): Foods, insect stings, medications, rapid onset of difficulty breathing, hypotension, urticaria, potentially fatal shock.
- Allergic Conjunctivitis: Pollen, other airborne allergens, redness, itching, tearing, swelling of the eyes.
Therapy
- Antihistamines: Block histamine (H1 receptors) reducing allergy symptoms.
- Corticosteroids: Suppress inflammation by inhibiting cytokine production.
- Decongestants: Reduce nasal swelling and congestion by vasoconstriction.
- Leukotriene Receptor Antagonists: Block leukotriene pathways, reducing bronchoconstriction and inflammation.
- Mast Cell Stabilizers: Prevent mast cell degranulation and reduce inflammatory mediators release.
- Epinephrine: Acts as a vasoconstrictor and bronchodilator, reversing severe systemic allergic reactions.
- Immunotherapy (Desensitization): Gradual exposure to increasing doses of allergens to reduce immune system sensitivity.
- Anti-IgE Therapy: Neutralizes IgE to prevent allergic reactions.
- Avoidance of Allergens: Minimizes exposure to known allergens.
Type II Hypersensitivity (Antibody-Mediated) Summary
- Caused by antibodies targeting antigens on cell surfaces or within tissues.
- Antigens can be endogenous (e.g., in cell membranes) or exogenous (e.g., drug metabolites).
- Mechanisms include opsonization and phagocytosis, complement activation and inflammation, and antibody-induced cellular dysfunction.
- Key examples are autoimmune hemolytic anemia, pemphigus, Goodpasture's syndrome.
- Therapies target inhibiting antibodies and reducing inflammation.
Goodpasture's Syndrome/Goodpasture's Disease Summary
- A systemic vasculitis caused by antibodies against basement membranes in the renal glomeruli and pulmonary alveoli.
- Characterized by rapidly progressive glomerulonephritis and diffuse alveolar hemorrhage.
- First described in 1919 by Ernest Goodpasture; the association with anti-basement membrane antibodies was discovered in 1965.
- Typically affects young white males under 40 years old, accounts for a significant proportion of RPGN diagnoses and leads to the risk of life-threatening pulmonary hemorrhage.
Type III Hypersensitivity (Immune Complex-Mediated) Summary
- Caused by immune complexes (antigen-antibody) deposition in tissues, triggering inflammation.
- Immune complexes form in circulation and are deposited in tissues (e.g., blood vessels, glomeruli, synovial membranes).
- Complement activation leads to inflammation and tissue damage.
- Important examples of this type of reaction include SLE, post-streptococcal glomerulonephritis, and serum sickness.
- Key features include the morphology (particularly in vasculitis and glomerulonephritis) and the common clinical presentations of the types of illnesses it can trigger (e.g., butterfly rash, kidney involvement).
Type IV Hypersensitivity (T Cell-Mediated) Summary
- Mediated by T cells, not antibodies.
- Two main mechanisms: delayed-type hypersensitivity (DTH) (CD4+ Th1 or Th17 cells) and direct cytotoxicity (CD8+ CTLs).
- DTH leads to chronic inflammation, while CTLs cause direct cell killing.
- Relevant clinical examples include contact dermatitis, type 1 diabetes, and tuberculosis.
Immune Tolerance Summary
- Tolerance is an essential ability for the immune system not to react against self-antigens.
- Mechanisms include elimination of, suppression of, and control of self-reactive lymphocytes during development and in periphery.
- Failure of these mechanisms can lead to autoimmune diseases or chronic inflammatory states such as immune-mediated inflammatory diseases.
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