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Questions and Answers
What initiates the degranulation process in mast cells during an allergic response?
Which phase of an allergic reaction involves the immediate release of histamine and cytokines?
What is the role of IL-4 in the sensitization process during an allergic reaction?
What characterizes Type I hypersensitivity reactions?
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What structural change occurs during the degranulation of mast cells?
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Which type of hypersensitivity is associated with autoimmune disorders?
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In Type II hypersensitivity, which component is primarily responsible for mediating cellular toxicity?
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What is the primary consequence of immune complex deposition in tissues during Type III hypersensitivity?
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What is the primary mechanism involved in Type II hypersensitivity reactions?
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Which autoimmune condition is an example of Type III hypersensitivity?
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How long after exposure do symptoms of Type IV hypersensitivity typically occur?
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What type of hypersensitivity is primarily characterized by T-cell activation and macrophage involvement?
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Which of the following is an example of Type I hypersensitivity?
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Which of the following mechanisms is NOT involved in the pathophysiology of Type II hypersensitivity reactions?
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What type of immune response is associated with alloimmunity?
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Which type of hypersensitivity is characterized by immune complex diseases?
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Which statement accurately describes the role of mast cells in allergic reactions?
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What is the major symptom of anaphylaxis in the context of Type I hypersensitivity?
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Which immunoglobulin is primarily associated with Type I hypersensitivity reactions?
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What is the duration of onset for Type II hypersensitivity reactions?
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What is the primary mechanism by which haptens lead to delayed type hypersensitivity (DTH) in contact dermatitis?
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Which of the following autoimmune diseases is associated with molecular mimicry involving Campylobacter jejuni?
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In the context of Type IV hypersensitivity disorders, which of the following is a characteristic feature of effector phase activation?
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Which antigen is targeted in Celiac Disease during Type IV hypersensitivity?
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What role do Langerhans cells play in the immune response related to Type IV hypersensitivity?
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Which of the following factors is NOT recognized as a risk factor for autoimmune diseases?
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What is a common characteristic of systemic lupus erythematosus (SLE)?
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In Type I diabetes, what primarily persists after the onset of the disease?
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Which type of hypersensitivity disorder is essentially mediated by immune complexes?
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What is the main immunological action taken by TH1 cells in the context of Type IV hypersensitivity?
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Study Notes
Hypersensitivity Reactions
- An altered immune response to an antigen leading to disease or damage to the host.
- Classified by mechanisms of disease (Type I-IV) or source of antigens:
- Allergy: over-reactivity to environmental antigens
- Autoimmunity: reaction to self-antigens
- Alloimmunity: reaction to tissues of another individual
Gell and Coombs Classification
- Type I: IgE-mediated, classic allergy, onset within minutes.
- Type II: IgG/IgM-mediated, cytotoxic reactions, onset in hours to days.
- Type III: IgG/IgM-mediated, immune-complex diseases, onset in hours to weeks.
- Type IV: T cell-mediated, delayed type hypersensitivity, onset in 2-3 days.
Type I Hypersensitivity: Allergy
- Mediated by IgE attached to mast cells.
- Symptoms: anaphylaxis, including hay fever, asthma, eczema, bee stings, food allergies.
- Systemic anaphylaxis is a medical emergency.
- Sensitization: repeated exposure to allergens is needed for class switching to IgE.
- Effector Stage: IgE receptor (FceR1) found on mast cells, basophils, and activated eosinophils.
- Degranulation: allergen binds IgE/FceR1 on mast cells, triggering Ca++ influx and release of inflammatory mediators.
- Immediate Phase: release of histamine and cytokines from mast cells, occurs within minutes.
- Late Phase: induction of eicosanoids, cytokines, and chemokines, immune cell infiltration, may last hours to days.
Allergens
- Small molecules, low doses can trigger a response.
- Common routes of exposure: airway, GI, urogenital.
Type I Hypersensitivity Reactions: Localized Anaphylaxis
- Target organ responds to direct contact with allergens.
- Examples:
- Lung: asthma, wheezing, dyspnea.
- Nose/Eyes: rhinitis, "hay fever", running nose, itchiness.
- Skin: urticaria, "hives", itchiness, blisters.
- GI tract: allergic gastroenteropathy, vomiting, diarrhea.
Type I Hypersensitivity Reactions: Systemic Anaphylaxis
- Systemic vasodilation and smooth muscle contraction leads to bronchiole constriction, edema, and hypotension.
- Symptoms: tachycardia, arrhythmia, cyanosis, cardiac arrest.
- Biphasic presentations are common (up to 30% of cases).
Type I Hypersensitivity Reactions: Genetic Predisposition
- Atopy is associated with a genetic predisposition for localized anaphylaxis.
- Atopic individuals have higher levels of IgE and eosinophils.
- Candidate genes: IL-4 receptor, IL-4 cytokine, FceRI, Class II MHC, inflammation genes.
Type II: Cytotoxic Hypersensitivity
- Mediated by IgG or IgM binding to a tissue cell surface antigen.
- Examples:
- ABO hemolytic anemia (blood transfusion errors)
- Auto-immune hemolytic anemia (autoimmune disease)
- Guillain Barre Syndrome (viral infection-induced)
- Special Type II reactions (Type V in the UK) target cell surface receptors.
Type III Hypersensitivity: Immune Complex Disease
- IgG or IgM antibodies bind soluble antigens, forming immune complexes (ICs).
- ICs are normally cleared by phagocytes.
- Undigested ICs deposit in tissues, causing inflammation and tissue injury.
- Examples:
- Glomerulonephritis (streptococcal infection)
- Rheumatoid arthritis (autoimmune)
- Systemic lupus erythematosus (autoimmune)
Type IV Hypersensitivity: Delayed Type Hypersensitivity (DTH)
- T-cell mediated inflammatory conditions.
- Implicated in some autoimmune diseases.
- Soluble protein antigens are presented by macrophages or dendritic cells to TH1 helper T-cells.
- TH1 cells release cytokines to recruit mononuclear cells and form granulomas.
- Examples:
- Contact dermatitis (effector phase: cytotoxic T cells)
- Tuberculin formation in tuberculosis (effector phase: TH1-macrophage)
Autoimmune Disorders
- Causes:
- Breakdown of immune tolerance against self-antigens.
- Molecular mimicry of infectious microbe antigens.
- Neo-antigen creation: altered protein structures.
- Risk Factors:
- Genetics: Polymorphic forms of MHC class II.
- Sex: hormonal, X-inactivation.
- Infections in susceptible individuals.
- Age: immunosenescence, loss of immune regulation.
Autoimmune Disease Examples
- Guillain Barre: Type II, gangliosides on nerve cells, PNS molecular mimicry.
- Graves Disease: Type II, thyroid stimulating hormone receptor, auto-antibodies activate thyroid.
- Myasthenia Gravis: Type II, nicotinic acetylcholine receptors, block muscle contractions.
- Rheumatoid Arthritis: Type III, synovial membrane, systemic autoimmunity and immune complexes.
- Systemic Lupus Erythematosus: Type III, anti-nuclear antibodies, systemic attacks.
- Celiac Disease: Type IV, gliadin-enterocytes, T-cell response to gluten.
- Multiple Sclerosis: Type IV, myelinated axons, CNS demyelination.
- Type I Diabetes: Type IV, insulin-producing beta cells, auto-antibodies against beta cells persist.
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Description
This quiz explores hypersensitivity reactions, including their classifications and mechanisms as per the Gell and Coombs system. Delve into the specific types, particularly Type I hypersensitivity, and understand the implications of allergic responses. It covers definitions, symptoms, and the importance of sensitization in allergic reactions.
