immuunontsnapping

Immune escape, or immuunontsnapping in Dutch, describes the strategies by which a pathogen, tumor, or other abnormal entity avoids detection or destruction by the host immune system. It is a central concept in immunology, infectious disease, and cancer biology, and can enable persistent infection or tumor progression.

Common mechanisms include antigenic variation, which changes surface proteins to evade antibodies and T cells; downregulation of major histocompatibility complex (MHC) molecules, reducing antigen presentation; and masking or modifying pathogen-associated molecular patterns to evade innate sensing. Additional strategies involve creating an immunosuppressive microenvironment through cytokines such as IL-10 and TGF-beta, or by recruiting regulatory T cells. Tumors may express programmed death-ligand 1 (PD-L1) to inhibit T cell activity, or escape by latency in immune-privileged sites. Some agents adopt dormancy, while others mimic host molecules to avoid recognition.

Examples include pathogens such as HIV, influenza, and herpesviruses, which show immune escape through mutation, drift, or latency. In cancer, immune escape is a hallmark of tumor evolution; cancer cells may downregulate MHC or upregulate checkpoint ligands, influencing response to therapies. Understanding immune escape has implications for vaccine design, antiviral strategies, and cancer immunotherapy.

Clinical relevance extends to treatment resistance and disease progression, motivating approaches that aim to restore immune recognition, such as checkpoint inhibitors, adoptive cell therapies, and combination regimens. Ongoing research seeks to map escape pathways, improve surveillance, and tailor interventions to counteract immune evasion across infections and malignancies.