Immune effector mechanisms damage host tissue as an unavoidable side effect of destroying pathogens. A response that is too broad, too strong, or too long converts a protective mechanism into a cause of disease.
Why effectors cannot be perfectly selective
A cytotoxic T cell recognizes its target through a specific peptide displayed on MHC class I. Any cell displaying that peptide is killed, regardless of whether it is infected. Inflammatory mediators such as tumor necrosis factor and reactive oxygen species are released into the extracellular space and act on whatever cells they reach. The precision of antigen recognition limits but does not eliminate this bystander damage.
The threshold logic
Because every response has a cost, the immune system is tuned to activate only when the threat is real and to stop when it is resolved. This is why activation requires multiple confirmatory signals rather than a single antigen encounter, and why termination is an active process rather than simple decay.