Immune Disorders: Hypersensitivity and Autoimmunity

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Immune Disorders

Overview of Hypersensitivity and Autoimmunity

Immune disorders arise when the immune system responds inappropriately, either by overreacting to harmless antigens (hypersensitivity) or by attacking the body’s own tissues (autoimmunity). Understanding these responses is crucial for diagnosing and treating related diseases.

Types of Hypersensitivity Reactions

Classification and Key Characteristics

Hypersensitivity reactions are classified into four types based on their mechanisms, timing, and cellular mediators. Each type is associated with distinct clinical manifestations and underlying immunological processes.

Descriptive	Name	Cause	Time Course	Characteristic Cells Involved
Type I	Immediate hypersensitivity	Antibody (mainly IgE) on sensitized cells interacts with antigen, causing degranulation	After initial sensitization, seconds to minutes	Previously sensitized mast cells or basophils
Type II	Cytotoxic hypersensitivity	Antibodies and complement lyse target cells	Minutes to hours	Plasma cells secrete antibodies that act against other body cells
Type III	Immune complex–mediated hypersensitivity	Nonphagocytized complexes of antibody and antigen trigger complement activation, leading to inflammatory damage	Several hours	Neutrophils
Type IV	Delayed (cell-mediated) hypersensitivity	T cells attack the body’s cells	Several days	Activated T cells

Table summarizing the four types of hypersensitivity reactions

Type I (Immediate) Hypersensitivity

Type I hypersensitivity, also known as immediate or anaphylactic hypersensitivity, is characterized by a rapid allergic reaction following exposure to an allergen. This response is mediated by IgE antibodies and involves mast cell or basophil degranulation, releasing inflammatory mediators such as histamine.

Key Features: Rapid onset (seconds to minutes), involves allergens, and can be localized (e.g., hay fever) or systemic (e.g., anaphylaxis).
Mechanism: Sensitization occurs upon first exposure; subsequent exposures trigger degranulation and mediator release.
Examples: Allergic rhinitis, asthma, food allergies, anaphylactic shock.

Diagram of sensitization in Type I hypersensitivity Diagram of degranulation in Type I hypersensitivity

Type II (Cytotoxic) Hypersensitivity

Type II hypersensitivity involves the destruction of cells by antibodies (IgG or IgM) and complement. This reaction is often seen in blood transfusion incompatibilities and certain autoimmune diseases.

Key Features: Antibody-mediated cell destruction, complement activation, and phagocytosis.
Examples: Hemolytic transfusion reactions, hemolytic disease of the newborn (Rh incompatibility).

ABO blood group compatibility table Diagram of transfusion reaction and hemolysis Diagram of Rh incompatibility in pregnancy

Type III (Immune Complex–Mediated) Hypersensitivity

Type III hypersensitivity is caused by the formation of immune complexes (antigen-antibody complexes) that are not efficiently cleared. These complexes deposit in tissues, triggering inflammation and tissue damage.

Key Features: Immune complex deposition, complement activation, neutrophil recruitment.
Examples: Systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), glomerulonephritis.

Photograph of rheumatoid arthritis in hands

Type IV (Delayed or Cell-Mediated) Hypersensitivity

Type IV hypersensitivity is mediated by T cells rather than antibodies. The reaction develops over 12–24 hours and involves macrophage and T cell recruitment to the site of antigen exposure.

Key Features: Delayed onset, T cell-mediated, tissue damage due to cellular immune response.
Examples: Tuberculin skin test, contact dermatitis (e.g., poison ivy), graft rejection.

Photograph of contact dermatitis on the skin

Autoimmune Diseases

Overview and Causes

Autoimmune diseases occur when the immune system mistakenly targets self-antigens, leading to tissue damage and chronic inflammation. The exact causes are multifactorial, involving genetic, hormonal, and environmental factors.

Key Features: Loss of self-tolerance, production of autoantibodies or autoreactive T cells, chronic inflammation.
Examples: Type I diabetes, rheumatoid arthritis, multiple sclerosis, lupus.

Hypotheses for the Causes of Autoimmunity

Several hypotheses have been proposed to explain the development of autoimmune diseases:

Estrogen may stimulate destruction of tissue by cytotoxic T cells.
Maternal or fetal cells crossing the placenta may trigger autoimmunity.
Environmental factors such as viral infections can initiate autoimmunity.
Genetic predisposition, especially certain MHC genes.
T cells may encounter self-antigens that are normally hidden.
Molecular mimicry by microorganisms may trigger autoimmunity.
Failure of normal immune regulation mechanisms.

Summary Table: ABO Blood Group Compatibility

ABO Blood Group	ABO Antigen(s) Present	Antibodies Present	Can Donate To	Can Receive From
A	A	Anti-B	A or AB	A or O
B	B	Anti-A	B or AB	B or O
AB	A and B	None	AB only	A, B, AB, or O (universal recipient)
O	None	Both anti-A and anti-B	A, B, AB, or O (universal donor)	O only

ABO blood group compatibility table

Key Points for Exam Preparation

Know the four types of hypersensitivity, their mechanisms, and clinical examples.
Understand the immunological basis of autoimmune diseases and the main hypotheses for their causes.
Be able to interpret blood group compatibility and the consequences of mismatched transfusions.