Immune mechanisms play an integral role in tumor growth establishment and metastases. Immunoediting is a dynamic process which contributes to immuno surveillance to keep under control It is made up of three phases: 1) elimination, 2) equilibrium, and 3) escape.
1. Elimination: Most immunologically vulnerable tumour antigens may eliminate by elimination phase immune editing as host’s immune system is capable of recognizing these cells
2. Equilibrium: However, constant division can generate tumour cells with reduced immunogenicity that can evade the immune elimination because of the genetic instability. This state of production of new tumor cell variants balanced by the distraction has been dubbed “equilibrium”, during which the cancer cells continue to divide, accumulating mutational changes by chance or in response to immune-induced inflammation.
3. Escape: These processes gradually come to a situation where tumours are capable of reducing the capacity of the immune system, to eradicate them by achieving immune suppressive effects or by loss of target antigen expression. Consequently tumour escapes from immuno surveillance and progression of carcinogenesis will occur. Nonetheless, there may be conditions under which tumor cells are truly dormant, for example by induction of “senescence”. In this case, they would be likely to remain dormant permanently, as replicative senescence is generally believed to be irreversible.
Microbiome studies based on ‘omic’ technologies have provided the laboratory evidence on disease associated in metabolic diseases and cancer (non infectious origin). These microbes especially bacteria are the most metabolically versatile organisms in the world, which can adopt to any environment, even changing their genetic potential, using mechanisms such as horizontal gene transfer. Thus cancer associated microbiome dominated by inflammaphilic periodontopathogens can be found in OSCC tumour micro environment.Furthermore, in-vitro experiments have provided substantial information on carcinogenicity of P. gingivalis and F. nucleatum.
I would like to start a meaningful discussion on immune responses of the host to 'cancerbiome induced inflammation' which can retard the 'immuno surveillance ' in oral carcinogenesis. For an example , retardation of 1st and 2 nd steps in immuno editing, which may cause immuno suppression, where tumour could escape from immuno surveillance. For an example well known periodonto pathogens such as P. gingivalis or F. nucleatum., how they can contribute to immuno suppression of the host which may lead tumour cells to escape from immuno surveillance ?
It's just a matter of combining information in the article 'The Microbiome of Oral Squamous Cell Carcinomas: a Functional Perspective' with the other article 'New insights into cancer immunoediting and its three component phases — elimination, equilibrium and escape'
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