Stress-induced self-antigens

"Stress-induced self-antigens" describes a biological phenomenon where the body's own proteins become antigenic under conditions of cellular stress (e.g., infection, malignancy, hypoxia, damage). These molecules are typically not recognized as foreign but undergo upregulation, conformational changes, or altered localization, making them visible to the immune system. Examples include NKG2D ligands (MICA, MICB, ULBP proteins) involved in NK cell killing, and ribonucleoprotein complexes like Ro/SSA and La/SSB, or chaperones like calreticulin and Grp78/BiP, which are implicated in autoimmune diseases. This concept is not a single, well-defined molecular target for drug development, but rather a heterogeneous collection of molecules and mechanisms. Understanding this phenomenon is clinically relevant to cancer immunosurveillance and autoimmune disease pathogenesis, but therapeutic interventions would typically target specific antigens (e.g., NKG2D ligands) or their recognition pathways rather than the broad category of "stress-induced self-antigens".