immunopathogenesis

Immunopathogenesis is the study of how immune responses contribute to the development and progression of disease. It describes the mechanisms by which components of the immune system—both innate and adaptive—can cause tissue injury and dysfunction, rather than protecting the host alone. Immunopathogenesis is relevant to infections, autoimmune disorders, hypersensitivity reactions, and transplant biology, among other contexts.

Damage can arise through several pathways. Immune complexes formed by antibodies and antigens can deposit in tissues and activate complement, leading to inflammation and injury. Autoimmune diseases involve autoreactive B and T cells that target self-tissues, producing antibodies or cytotoxic responses that cause organ-specific or systemic damage. Cytokines and chemokines can recruit and activate inflammatory cells, producing collateral tissue injury. Antibody-dependent cellular cytotoxicity and direct T cell–mediated cytotoxicity can destroy infected or normal cells. In infections, the immune response may help clear pathogens but also contribute to pathology, as seen in dengue, influenza, or severe COVID-19 cases. Hypersensitivity reactions (types I–IV) illustrate distinct immunopathogenic processes, including allergic inflammation and delayed-type hypersensitivity. Transplant rejection results from recognition of foreign antigens by T cells and antibodies, leading to graft injury.

Genetic predisposition, environmental triggers, and failures of regulation influence susceptibility and severity. Concepts such as molecular mimicry, epitope spreading, bystander activation, and regulatory dysfunction help explain how immune tolerance can break down. Understanding immunopathogenesis informs therapeutic approaches that modulate immune responses, including immunosuppressants and targeted biologic agents, with the aim of reducing immune-mediated tissue damage while preserving host defense.