Chapter 21 - Section 21.6 - Immune System Disorders - Before You Go On - Page 841: 25

Delayed hypersensitivity, also known as Type IV hypersensitivity, differs from acute and subacute types in several key aspects beyond the time required for the reaction to appear. Let's explore these differences: 1. **Underlying Mechanism:** - Acute Hypersensitivity (Type I): Involves an immediate immune response triggered by the release of histamines and other inflammatory mediators from mast cells and basophils. - Subacute Hypersensitivity (not a widely recognized term): There isn't a well-defined distinction between this and acute hypersensitivity, but it might imply a somewhat milder or less immediate reaction compared to Type I hypersensitivity. - Delayed Hypersensitivity (Type IV): Involves a delayed immune response mediated by T cells, particularly CD4+ helper T cells and CD8+ cytotoxic T cells. Macrophages are also involved. This type of response takes time to develop (usually 24-72 hours) after exposure to the antigen. 2. **Clinical Presentation:** - Acute Hypersensitivity: Often presents with rapid-onset symptoms like itching, hives, swelling, and in severe cases, anaphylaxis. Examples include allergic reactions to foods, insect stings, and medications. - Subacute Hypersensitivity: This term isn't well-defined, but if referring to a milder version of acute hypersensitivity, symptoms might be less severe and more delayed compared to Type I reactions. - Delayed Hypersensitivity: Typically presents as skin reactions, such as redness, swelling, and induration (hardening of tissue) at the site of exposure. Common examples include contact dermatitis (e.g., poison ivy) and tuberculin skin testing. 3. **Immune Cells Involved:** - Acute Hypersensitivity: Involves B cells, mast cells, basophils, and IgE antibodies. - Subacute Hypersensitivity: Not well-defined, but likely involves similar immune cells and mechanisms as acute hypersensitivity. - Delayed Hypersensitivity: Primarily mediated by T cells (both CD4+ and CD8+), and macrophages play a key role in the inflammatory response. 4. **Time Course:** - Acute Hypersensitivity: Rapid onset, typically within minutes to hours after exposure to the allergen. - Subacute Hypersensitivity: If interpreted as a milder form of acute hypersensitivity, the time course might be similar but with less severe and delayed symptoms. - Delayed Hypersensitivity: Takes 24-72 hours to develop after exposure, hence the term "delayed." 5. **Pathophysiology:** - Acute Hypersensitivity: Involves the cross-linking of allergen-specific IgE antibodies on the surface of mast cells and basophils, leading to the release of histamines and other inflammatory mediators. - Subacute Hypersensitivity: Likely follows a similar pathophysiology to acute hypersensitivity but might involve different thresholds or sensitivities. - Delayed Hypersensitivity: Involves T cell recognition of antigens presented by antigen-presenting cells (APCs) like macrophages. This activates a cellular immune response that recruits more immune cells to the site of exposure, causing inflammation. In summary, delayed hypersensitivity (Type IV) is fundamentally distinct from acute hypersensitivity (Type I) in terms of immune mechanisms, time course, clinical presentation, and the types of immune cells involved. Subacute hypersensitivity is not a widely recognized term and might be interpreted as a milder form of acute hypersensitivity with delayed symptoms.

Delayed hypersensitivity, also known as Type IV hypersensitivity, differs from acute and subacute types in several key aspects beyond the time required for the reaction to appear. Let's explore these differences: 1. **Underlying Mechanism:** - Acute Hypersensitivity (Type I): Involves an immediate immune response triggered by the release of histamines and other inflammatory mediators from mast cells and basophils. - Subacute Hypersensitivity (not a widely recognized term): There isn't a well-defined distinction between this and acute hypersensitivity, but it might imply a somewhat milder or less immediate reaction compared to Type I hypersensitivity. - Delayed Hypersensitivity (Type IV): Involves a delayed immune response mediated by T cells, particularly CD4+ helper T cells and CD8+ cytotoxic T cells. Macrophages are also involved. This type of response takes time to develop (usually 24-72 hours) after exposure to the antigen. 2. **Clinical Presentation:** - Acute Hypersensitivity: Often presents with rapid-onset symptoms like itching, hives, swelling, and in severe cases, anaphylaxis. Examples include allergic reactions to foods, insect stings, and medications. - Subacute Hypersensitivity: This term isn't well-defined, but if referring to a milder version of acute hypersensitivity, symptoms might be less severe and more delayed compared to Type I reactions. - Delayed Hypersensitivity: Typically presents as skin reactions, such as redness, swelling, and induration (hardening of tissue) at the site of exposure. Common examples include contact dermatitis (e.g., poison ivy) and tuberculin skin testing. 3. **Immune Cells Involved:** - Acute Hypersensitivity: Involves B cells, mast cells, basophils, and IgE antibodies. - Subacute Hypersensitivity: Not well-defined, but likely involves similar immune cells and mechanisms as acute hypersensitivity. - Delayed Hypersensitivity: Primarily mediated by T cells (both CD4+ and CD8+), and macrophages play a key role in the inflammatory response. 4. **Time Course:** - Acute Hypersensitivity: Rapid onset, typically within minutes to hours after exposure to the allergen. - Subacute Hypersensitivity: If interpreted as a milder form of acute hypersensitivity, the time course might be similar but with less severe and delayed symptoms. - Delayed Hypersensitivity: Takes 24-72 hours to develop after exposure, hence the term "delayed." 5. **Pathophysiology:** - Acute Hypersensitivity: Involves the cross-linking of allergen-specific IgE antibodies on the surface of mast cells and basophils, leading to the release of histamines and other inflammatory mediators. - Subacute Hypersensitivity: Likely follows a similar pathophysiology to acute hypersensitivity but might involve different thresholds or sensitivities. - Delayed Hypersensitivity: Involves T cell recognition of antigens presented by antigen-presenting cells (APCs) like macrophages. This activates a cellular immune response that recruits more immune cells to the site of exposure, causing inflammation. In summary, delayed hypersensitivity (Type IV) is fundamentally distinct from acute hypersensitivity (Type I) in terms of immune mechanisms, time course, clinical presentation, and the types of immune cells involved. Subacute hypersensitivity is not a widely recognized term and might be interpreted as a milder form of acute hypersensitivity with delayed symptoms.