Immunology Chapter on Hypersensitivity Reactions

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Questions and Answers

What is the primary action of corticosteroids in hypersensitivity treatment?

Increase vascular permeability

Enhance immune cell activation

Reduce inflammation by inhibiting cytokine production (correct)

Promote cytokine production

What characterizes SRS-A (slow-reacting substance of anaphylaxis)?

It is an antibody-mediated response

It is a group of leukotrienes causing prolonged smooth muscle contraction (correct)

It enhances vascular permeability only

It causes rapid smooth muscle relaxation

What is the definition of anaphylaxis?

A temporary skin irritation caused by contact with an allergen.

A severe, life-threatening systemic allergic reaction. (correct)

A mild allergic reaction characterized by a rash.

A chronic condition of the respiratory system.

Which function does serotonin serve during anaphylaxis?

Induces vasoconstriction of large blood vessels and vasodilation of capillaries Signup and view all the answers

Which type of hypersensitivity is mediated by IgE antibodies?

Type I hypersensitivity Signup and view all the answers

How do leukotrienes contribute to the pathophysiology of asthma?

Cause bronchoconstriction and increased vascular permeability Signup and view all the answers

What occurs during the process of sensitization?

Formation of antibodies without an immediate reaction. Signup and view all the answers

What distinguishes an anaphylactoid reaction from anaphylaxis?

It is not mediated by IgE but by direct mast cell degranulation Signup and view all the answers

What characterizes Type IV hypersensitivity?

Delayed T-cell-mediated immune responses. Signup and view all the answers

What is an example of a Type II hypersensitivity reaction?

Hemolytic anemia Signup and view all the answers

What is the role of mast cells in immediate hypersensitivity reactions?

To release preformed mediators like histamine. Signup and view all the answers

What is the effector mechanism utilized in Type III hypersensitivity?

Complement activation and neutrophil recruitment Signup and view all the answers

Which cells are primarily mediators in Type IV hypersensitivity?

CD4+ and CD8+ T cells Signup and view all the answers

Which of the following is NOT a clinical manifestation of Type I hypersensitivity?

Rash associated with contact dermatitis Signup and view all the answers

Which mediator is primarily released during a Type I hypersensitivity reaction?

Histamine Signup and view all the answers

What role do macrophages play in Type IV hypersensitivity reactions?

Release cytokines leading to inflammation Signup and view all the answers

What does the tuberculin skin test assess?

Infection with tuberculosis Signup and view all the answers

What is desensitization in the context of allergies?

Creating tolerance by administering increasing doses of an allergen. Signup and view all the answers

What is a shocking dose in allergic reactions?

The amount of allergen that causes an allergic reaction in a sensitized individual. Signup and view all the answers

Which of the following statements about IgE is correct?

IgE binds to mast cells and basophils, causing degranulation upon allergen exposure. Signup and view all the answers

What causes contact allergy?

A delayed hypersensitivity reaction from skin contact with certain substances Signup and view all the answers

What is the primary allergen found in poison ivy?

Urushiol Signup and view all the answers

In autoimmune diseases like rheumatoid arthritis, what do T cells specifically attack?

Self-antigens in the body Signup and view all the answers

What characterizes Myasthenia gravis?

Antibodies blocking acetylcholine receptors Signup and view all the answers

How does Goodpasture's syndrome function at the immune level?

Antibodies attack the basement membranes of vital organs Signup and view all the answers

What role do leukotrienes play in asthma?

They are main mediators of bronchoconstriction Signup and view all the answers

What happens during chronic desensitization therapy?

Long-term administration of an allergen leading to IgG production Signup and view all the answers

What is the primary action of histamine during allergic reactions?

Increase in vascular permeability and smooth muscle contraction Signup and view all the answers

How do immune complexes lead to tissue damage in immune complex diseases?

Depositing in tissues and activating complement Signup and view all the answers

What triggers rheumatic fever in relation to hypersensitivity?

Cross-reactive antibodies against streptococcal bacteria and heart tissue Signup and view all the answers

Study Notes

Hypersensitivity Reactions

Allergy: Immune response to an antigen (allergen)
Anaphylaxis: Life-threatening allergic reaction with bronchoconstriction and hypotension.
Atopic: Genetic predisposition to allergies like asthma, hay fever, and eczema.
Sensitization: First contact with an antigen induces antibody formation without immediate reaction.
Desensitization: Gradual administration of allergen to reduce reactions.
Shocking Dose: Allergen dose causing reaction in a sensitized individual.
Hypersensitivity Types:
- Type I (Immediate): IgE-mediated
- Type II (Cytotoxic): IgG or IgM antibody-mediated
- Type III (Immune Complex): Immune complexes in tissues
- Type IV (Cell-Mediated): Delayed T-cell responses

Type I Hypersensitivity: Immediate

Mast Cells: Release histamine upon activation by IgE, causing allergic symptoms.
Degranulation: Release of preformed mediators (histamine, heparin, ECF-A, serotonin) by mast cells.
Primary mediator: Histamine
Newly synthesized mediators: Prostaglandins, leukotrienes, thromboxanes, SRS-A
IgE Role: Binds to mast cells and basophils, triggers degranulation upon allergen cross-linking.
Clinical Manifestations: Urticaria, eczema, conjunctivitis, rhinitis, asthma, anaphylaxis.
Epinephrine: Increases cAMP, inhibiting mediator release and relaxing smooth muscle.
Corticosteroids: Reduce inflammation by inhibiting cytokine production and stabilizing immune cells.
SRS-A (Slow-Reacting Substance of Anaphylaxis): Leukotrienes causing prolonged muscle contraction and vascular permeability.
Eosinophils: Release histaminase and arylsulfatase to degrade histamine and SRS-A, potentially reducing allergic reactions.
Serotonin: Causes vasoconstriction of large vessels and vasodilation of capillaries, contributing to the allergic response.
Leukotrienes in Asthma: Cause bronchoconstriction, increased vascular permeability, and inflammation.
Anaphylactoid Reaction: Similar to anaphylaxis but not IgE-mediated; caused by direct mast cell degranulation by certain drugs.
Prausnitz-Küstner Reaction: Historical test for allergy sensitivity by injecting serum from an allergic person into a non-allergic individual.
Drug Hypersensitivity: Rashes, fever, local or systemic anaphylaxis, varying severity.

Type II Hypersensitivity: Cytotoxic

Mechanism: IgG or IgM antibodies bind to cell surface antigens, leading to complement-mediated lysis or antibody-dependent cellular cytotoxicity (ADCC).
Example: Hemolytic anemia or ABO transfusion reactions.

Type III Hypersensitivity: Immune Complex-Mediated

Mechanism: Immune complexes form and deposit in tissues, activating complement and causing inflammation and tissue damage.
Autoimmune Disease Example: Systemic lupus erythematosus (SLE).
Effector Mechanism: Complement activation and neutrophil recruitment causing tissue injury.

Type IV Hypersensitivity: Cell-Mediated

Mechanism: Delayed T-cell-mediated immune responses.
Example: Contact dermatitis or tuberculin test.
Mediating Cells: CD4+ helper T cells and CD8+ cytotoxic T cells.
Macrophage Role: Activated by T cells to produce cytokines and cause inflammation at the site of antigen exposure.
Tuberculin Skin Test: Tests for previous exposure to Mycobacterium tuberculosis.
Contact Allergy: Delayed reaction caused by skin contact with chemicals, plant material, or cosmetics.
Poison Ivy Allergen: Urushiol, acting as a hapten causing contact dermatitis.

Autoimmune Diseases and Hypersensitivity

T Cells in Autoimmune Diseases: Attack self-antigens in tissues, leading to inflammation and tissue damage.
Myasthenia Gravis: Antibodies block acetylcholine receptors, causing muscle weakness.
Graves' Disease: Antibodies stimulate thyroid, causing hyperthyroidism.
Immune Complex-Mediated Diseases: Immune complexes persist and deposit in tissues, causing arthritis and nephritis.
Goodpasture's Syndrome: Antibodies attack basement membranes of kidneys and lungs, causing organ damage.
Rheumatic Fever: Antibodies against streptococcal bacteria cross-react with heart tissue, causing damage.
Pemphigus: Autoimmune skin disease with blisters due to antibodies attacking skin cells.

Key Mediators and Mechanisms

Histamine: Increases vascular permeability, vasodilation, and smooth muscle contraction.
Leukotrienes: Main mediators of bronchoconstriction, not treatable by antihistamines.
Complement: Activated by antibodies bound to antigens, leading to inflammation and cell lysis.
Chronic Desensitization Therapy: Long-term allergen administration leads to production of blocking IgG antibodies, preventing allergic reactions.

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Description

Test your knowledge on hypersensitivity reactions with this quiz. Explore the different types of hypersensitivity, including immediate and delayed responses, and learn about associated conditions like allergies and anaphylaxis. This quiz will challenge your understanding of immune responses to allergens and the mechanisms involved.