In medical terms, DTH stands for Delayed-Type Hypersensitivity, an immune reaction characterized by an inflammatory response that typically develops 24 to 72 hours after exposure to an antigen. This crucial immune response is primarily mediated by specialized immune cells known as T cells, rather than by antibodies (which are produced by B cells).
Understanding Delayed-Type Hypersensitivity (DTH)
DTH is a fundamental component of the adaptive immune system, representing a cell-mediated immunity pathway. It's an inflammatory reaction that signifies the body's recognition of a foreign substance, or antigen, which it has encountered previously.
The "Delayed" Aspect
The most defining characteristic of DTH is its delayed onset. Unlike immediate allergic reactions (like those to pollen or peanuts), which manifest within minutes, DTH reactions take 24 to 72 hours to reach their peak. This delay is due to the time required for specialized T cells to migrate to the site of antigen exposure, recognize the antigen, and initiate an inflammatory cascade.
Key Immune Players: T Cells
DTH reactions are predominantly orchestrated by T cells, specifically CD4+ helper T cells and CD8+ cytotoxic T cells.
- T cells are a type of white blood cell that play a central role in cell-mediated immunity. They are distinct from B cells, which produce antibodies. In DTH, T cells directly recognize and respond to the antigen, leading to inflammation and tissue damage.
- Antigens are substances (like proteins, carbohydrates, or chemicals) that the immune system perceives as foreign and potentially harmful.
How DTH Works: A Two-Phase Process
The development of a DTH reaction involves two main phases:
-
Sensitization Phase:
- Upon the initial exposure to an antigen, specialized antigen-presenting cells (APCs), such as dendritic cells, capture the antigen.
- These APCs then travel to lymph nodes, where they present the antigen to naive T cells.
- The T cells that recognize the antigen become activated, proliferate, and differentiate into memory T cells and effector T cells. This process takes approximately 1-2 weeks.
-
Elicitation Phase:
- During subsequent exposure to the same antigen, the previously sensitized memory and effector T cells are rapidly activated.
- These T cells migrate to the site of antigen exposure and release various cytokines.
- Cytokines attract and activate other immune cells, such as macrophages, which release inflammatory mediators, leading to the characteristic swelling, redness, and heat observed in DTH reactions.
Common Examples of DTH Reactions
DTH plays a significant role in various medical conditions and diagnostic tests:
- Tuberculin (Mantoux) Skin Test: This widely used diagnostic test for tuberculosis (TB) is a classic example of a DTH reaction. A small amount of tuberculin purified protein derivative (PPD) is injected into the skin. If the person has been previously exposed to TB bacteria, T cells will recognize the PPD, leading to a localized swelling and redness (induration) within 48-72 hours.
- Contact Dermatitis: This common skin inflammation occurs when the skin comes into contact with certain allergens. Examples include:
- Poison ivy/oak: The urushiol oil in these plants triggers a DTH reaction.
- Nickel allergy: Contact with nickel jewelry or objects can cause a rash.
- Latex allergy: In some individuals, latex exposure can cause DTH.
- Cosmetics and fragrances: Certain ingredients can lead to delayed skin reactions.
- Granuloma Formation: In chronic infections (e.g., TB, leprosy, fungal infections) or foreign body reactions, persistent DTH can lead to the formation of granulomas, which are organized collections of immune cells attempting to wall off the offending agent.
Clinical Significance and Diagnosis
Understanding DTH is crucial for both diagnosis and managing various conditions:
- Diagnostic Tool: Skin tests, like the Mantoux test, leverage the DTH mechanism to detect prior exposure to specific pathogens or allergens.
- Disease Pathology: DTH contributes to the tissue damage seen in autoimmune diseases, chronic infections, and organ transplant rejection.
- Identifying Allergens: Patch testing for contact dermatitis helps identify specific allergens by observing delayed skin reactions.
Distinguishing DTH from Other Hypersensitivity Reactions
It's important to differentiate DTH (Type IV hypersensitivity) from other types of hypersensitivity reactions. The table below highlights key differences between DTH and Immediate Hypersensitivity (Type I):
| Feature | Delayed-Type Hypersensitivity (DTH) | Immediate Hypersensitivity (Type I) |
|---|---|---|
| Onset | 24-72 hours post-exposure | Minutes to a few hours post-exposure |
| Primary Immune Mediators | T cells (e.g., CD4+ helper T cells, CD8+ cytotoxic T cells) | Antibodies (specifically IgE) and mast cells |
| Mechanism | Cell-mediated; T cells directly interact with antigen and release cytokines | Antibody-mediated; IgE antibodies trigger mast cell degranulation and histamine release |
| Examples | Tuberculin test, contact dermatitis (e.g., poison ivy, nickel allergy) | Hay fever, allergic asthma, food allergies, anaphylaxis |
Managing DTH Reactions
Management strategies for DTH reactions primarily focus on:
- Avoidance: Identifying and avoiding the offending antigen is the most effective way to prevent reactions, especially in contact dermatitis.
- Topical Corticosteroids: For localized skin reactions, anti-inflammatory creams or ointments containing corticosteroids can reduce swelling, redness, and itching.
- Systemic Corticosteroids: In severe or widespread DTH reactions, oral corticosteroids may be prescribed to suppress the immune response.
By understanding the mechanisms and implications of Delayed-Type Hypersensitivity, medical professionals can accurately diagnose and effectively manage a range of immune-mediated conditions.
