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Hypersensitivity, Autoimmunity, and Immunodeficiency: Immune System Disorders

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Chapter 17: Immune System Disorders

Introduction

This chapter explores how the immune system, while protective, can also cause harm if its responses are uncontrolled or misdirected. The main focus is on hypersensitivity reactions, autoimmune diseases, and immunodeficiency disorders.

Glimpse of History: Discovery of Anaphylaxis

  • Charles Richet and Paul Portier studied toxins from marine organisms such as the Portuguese man-of-war jellyfish and sea anemones.

  • They observed that animals exposed to a small second dose of toxin weeks after an initial exposure died rapidly, indicating a destructive immune response.

  • This phenomenon was termed anaphylaxis, a severe, rapid allergic reaction.

  • Richet received the Nobel Prize in 1913 for this discovery.

Immune System: Protective and Potentially Harmful

  • Hypersensitivity: An immune response that injures tissues.

  • Allergy: Sensitivity to an allergen (a normally harmless environmental substance), usually involving an IgE response.

  • Autoimmune disease: The immune system targets the body’s own tissues.

  • Immunodeficiency: The immune system is too weak to prevent infection.

Classification of Hypersensitivity Reactions

Hypersensitivity reactions are categorized into four major types based on their mechanisms and timing:

Type

Immune Component

Effector Mechanism

Onset

Examples

Type I Immediate IgE-Mediated

B cells, IgE

Mast cells, basophils, release of histamine and other mediators

Immediate (within minutes)

Allergic reactions (hay fever, asthma, anaphylaxis)

Type II Cytotoxic

B cells, IgG, IgM

Complement activation, ADCC (NK cells)

Hours to days

Transfusion reactions, hemolytic disease of the newborn

Type III Immune Complex-Mediated

B cells, IgG, IgM

Immune complex deposition, complement, neutrophils

Hours to days

Serum sickness, Arthus reaction, lupus

Type IV Delayed-Type Cell-Mediated

T cells

Macrophage activation, cytotoxic T cells

Peaks at 48–72 hours

Contact dermatitis, tuberculin reaction, transplant rejection

Key Terms and Concepts

  • IgE: Immunoglobulin E, an antibody class involved in allergic responses.

  • Mast cells: Cells that release histamine and other mediators during allergic reactions.

  • Basophils: White blood cells that participate in inflammatory and allergic responses.

  • Complement system: A group of proteins that enhance immune responses, especially in cytotoxic and immune complex-mediated hypersensitivities.

  • ADCC (Antibody-Dependent Cellular Cytotoxicity): A mechanism where NK cells destroy antibody-coated target cells.

  • Immune complex: Aggregates of antigens and antibodies that can deposit in tissues and cause inflammation.

  • Delayed-type hypersensitivity: A T cell-mediated immune response that peaks several days after antigen exposure.

Examples and Applications

  • Type I Example: Hay fever, asthma, and anaphylactic shock are classic IgE-mediated allergic reactions.

  • Type II Example: Transfusion of incompatible blood types can cause cytotoxic reactions leading to cell lysis.

  • Type III Example: Systemic lupus erythematosus (SLE) involves immune complex deposition in tissues.

  • Type IV Example: Tuberculin skin test and contact dermatitis (e.g., poison ivy) are mediated by T cells.

Additional info: The table above is a logical reconstruction based on the visible slide and standard textbook content for this topic.

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