Release-killing mechanisms

Host cells are killed by cytotoxic T-ceUs or natural kiUer cells by the processes of necrosis or apoptosis. Necrosis leads to release of cell contents that can sufficiently disturb the tissue to initiate a local inflammatory response. However, the cell killed by apoptosis is then phagocytosed, which does not cause local disturbance, so that inflammation does not occur (Chapter 20). Apoptosis is achieved by two mechanisms release of toxic granules by the cytotoxic cells or by the binding of the cytotoxic ceU to the host ceU, via its death receptor protein (see below). 

The first contact-killing surface was described by Isquith et al., who modified glass substrates with the silane 3-(trimethoxysilyl)-propyldimethyloctadecylammonium chloride, often referred to as DOW5700 [39], However, the claim was made on the basis of the DOW suspension test (see Sect. 2.2), which cannot distinguish between biocide release and contact activity. In subsequent work, neither the original authors nor followers proposed a working model for a mechanisms that was able to explain the contact activity of this surface modification. The first model for contact activity was proposed in 2001 (see Fig. 5) [40],... 

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