Cell coat

NK cells possess a receptor for Fc/and this enables them to adhere to target cells coated in antibody with the resultant destruction ofthat cell. This phenomenon is known as antibody-dependent cell-mediated cytotoxicity (ADCC). This was attributed to a separate cell population known as killer (K) cells but these have now been shown to be in effect NK cells. 

Drugs frequently bind to blood elements directly (e.g. penicillin to erythrocytes) and the antibodies to the resultant complex react with, and damage, cells coated with the drug. Viruses, especially those that bud, become associated with the host cell surface antigens with the resultant generation of Tc cells. 

Although a few mechanisms have so far been proposed to explain the antimicrobial properties exhibited by proanthocyanidins (e.g., inhibition of extracellular enzymes) [86], Jones et al. [83] postulated that their ability to bind bacterial cell coat polymers and their abihty to inhibit cell-associated proteolysis might be considered responsible for the observed activity (Table 1). Accordingly, despite the formation of complexes with cell coat polymers, proanthocyanidins penetrated to the cell wall in sufficient concentration to react with one or more ultra-structural components and to selectively inhibit cell wall synthesis. Decreased proteolysis in these strains may also reflect a reduction of the export of proteases from the cell in the presence of proanthocyanidins [83]. 

Shan, G. B. Xing, J. M. Zhang, H. Y., and Liu, H. Z., Biodesulfurization of dibenzothio-phene by microbial cells coated with magnetite nanoparticles. Applied and Environmental Microbiology, 2005. 71(8) p. 4497. 

The glycocalyx (carbohydrate-rich outer cell coat) can possibly shield tumour antigens from the immune system. 

Nitta, T, K. Sato, K. Okumura, and S. Ishii, Induction of cytotoxicity in human T cells coated with anti-glioma x anti-CD3 bispecific antibody against human glioma cells. J Neurosurg, 1990. 72(3) 476-81. 

The cell coat of trypanosomes is covered with a single protein, which is the antigen to which the immune system responds. Every so often, however, by a process of genetic recombination (see Table 28-1), a few cells in the population of infecting trypanosomes switch to a new protein coat, not recognized by the immune system. This process of changing coats can occur hundreds of times. The result is a chronic cyclic infection the human host develops a fever, which subsides as the immune system beats back the first infection trypanosomes with changed coats then become the seed for a second infection, and the fever recurs. This cycle can repeat for weeks, and the weakened person eventually dies. 

While some organisms promote mineral deposition completely outside of their cell coats, the mineralization is usually controlled by the proteins and polysaccharides lying around and between cells.683-687... 

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