过敏反应：迟发型超敏反应

Delayed hypersensitivity consists of sensitization and effector phases. During sensitization, antigen-presenting cells activate CD4+ TH1 cells via MHC class II molecules, leading to clonal expansion of antigen-specific effector T cells. Upon re-exposure, the effector phase begins, where sensitized TH1 cells release cytokines like IFN-γ and TNF-α, recruiting and activating macrophages that cause tissue inflammation and damage.

Recruited macrophages exhibit increased phagocytic activity and release lytic enzymes that directly damage tissue. They also produce cytokines and chemokines that attract additional monocytes and neutrophils to the inflammation site. This amplification of the immune response intensifies tissue damage and inflammation, particularly during the effector phase when macrophage activation peaks 48-72 hours after antigen exposure.

Antigen-presenting cells such as macrophages, dendritic cells, and Langerhans cells transport antigens to lymph nodes during the sensitization phase. There, they present antigens to CD4+ T cells via MHC class II molecules, initiating T cell activation and clonal expansion. This process establishes the foundation for the delayed immune response by generating mature effector T cells that recognize the antigen upon re-exposure.

Contact dermatitis occurs when reactive chemicals from plants or metals bind to skin proteins, creating neoantigens. These modified proteins sensitize T cells, triggering cytokine release and inflammatory cell recruitment. The delayed onset and cell-mediated mechanism involving T cell activation and macrophage recruitment classify it as a Type IV hypersensitivity reaction, exemplifying how hapten-protein complexes generate immune responses.

Prolonged delayed hypersensitivity can cause granulomatous reactions characterized by granuloma formation in body tissues. Continuous macrophage activation leads to multinucleated giant cell formation, ultimately resulting in tissue necrosis. These chronic inflammatory responses represent an amplified version of the standard delayed hypersensitivity mechanism, where persistent antigen exposure and macrophage activation cause extensive tissue destruction.

Delayed hypersensitivity reactions have a characteristic 1-2 day onset, with peak response occurring 48-72 hours after antigen re-exposure. This delayed timeline contrasts with antibody-mediated responses that occur within minutes to hours. The lag reflects the time required for T cell recruitment, macrophage activation, and cytokine-mediated inflammation to develop fully at the reaction site.

TH1 effector cells release key cytokines including interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and lymphotoxin-α during the effector phase. These cytokines recruit and activate macrophages at the inflammation site, amplifying the immune response. The coordinated release of these mediators drives the complex interplay of nonspecific cells and mediators characteristic of delayed hypersensitivity reactions.