In type IV hypersensitivity, which immune cell type is primarily involved?

In type IV hypersensitivity, which immune cell type is primarily involved?

• A. B cells
• B. NK cells
• C. T cells
• D. Neutrophils

Answer: (C)

Type IV hypersensitivity is driven by T cell–mediated immunity, not antibodies. The main players are T lymphocytes, especially CD4+ helper T cells (often Th1) that release IFN-γ to activate macrophages, leading to the macrophage-driven inflammation and tissue damage seen in delayed-type reactions like contact dermatitis or the tuberculin skin test. CD8+ cytotoxic T cells can contribute by killing antigen-bearing cells, but the hallmark of this hypersensitivity is the T cell–mediated activation of other immune cells, not antibody actions. B cells produce antibodies and drive antibody-mediated (types I–III/II) responses, so they are not the primary effectors here. NK cells are innate cytotoxic cells that act early in viral infections and some antibody-dependent contexts, not the central mediators of type IV. Neutrophils participate in the inflammatory cascade but are not the primary orchestrators of this delayed-type, T cell–driven reaction.

Type IV hypersensitivity is driven by T cell–mediated immunity, not antibodies. The main players are T lymphocytes, especially CD4+ helper T cells (often Th1) that release IFN-γ to activate macrophages, leading to the macrophage-driven inflammation and tissue damage seen in delayed-type reactions like contact dermatitis or the tuberculin skin test. CD8+ cytotoxic T cells can contribute by killing antigen-bearing cells, but the hallmark of this hypersensitivity is the T cell–mediated activation of other immune cells, not antibody actions.

B cells produce antibodies and drive antibody-mediated (types I–III/II) responses, so they are not the primary effectors here. NK cells are innate cytotoxic cells that act early in viral infections and some antibody-dependent contexts, not the central mediators of type IV. Neutrophils participate in the inflammatory cascade but are not the primary orchestrators of this delayed-type, T cell–driven reaction.