TypIVÜberempfindlichkeit

Type IV hypersensitivity, also known as delayed-type hypersensitivity (DTH), is a cell-mediated immune reaction in which sensitized T lymphocytes orchestrate inflammation and tissue injury in response to antigen. Unlike antibody-mediated hypersensitivities, it is driven by T cells rather than circulating antibodies. The principal effector cells are CD4+ Th1 and Th17 cells, and in some contexts CD8+ cytotoxic T lymphocytes. After initial exposure (sensitization), antigen-presenting cells process the antigen and present peptides to T cells in lymph nodes, generating memory T cells. Upon re-exposure, memory T cells recognize the antigen and secrete cytokines such as IFN-γ, IL-2, and TNF-α, recruiting and activating macrophages and other inflammatory cells, leading to tissue damage. If antigen persists, granulomatous inflammation may develop as macrophages differentiate and coalesce.

Common clinical examples include contact dermatitis from metals, cosmetics, poison ivy/oak, or fragrances; the tuberculin skin test (Mantoux) and other delayed-type skin reactions; granulomatous infections such as tuberculosis and certain fungal infections; and chronic graft-versus-host disease. Histology typically shows mononuclear infiltrates with macrophages, and granuloma formation in persistent cases.

Diagnosis relies on clinical history and targeted skin or intradermal tests (e.g., patch testing for contact allergens; tuberculin testing for latent infection). Management focuses on removing the offending antigen, applying topical or systemic corticosteroids to reduce inflammation, and, when needed, immunomodulatory therapies; infections requiring specific treatment should be addressed.

In German medical terminology, it is referred to as Typ-IV-Überempfindlichkeit.