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Tumor inhibitory T cell immunity may be largely a transplantation artifact not necessarily dependent upon a lack of Tregs.

Prehn RT, Prehn LM - Theor Biol Med Model (2013)

Bottom Line: There exists a very large literature suggesting that T cells come in a variety of species and that without the action of Tregs tumors would seldom survive inhibition by T cell effectors.We believe that much of the evidence supporting the role of Tregs in cancer is compatible with a perhaps simpler hypothesis based upon the demonstration that that small quantities of effector T cells tend to stimulate tumors while larger quantities of seemingly the same cells are inhibitory (an hormesis-like effect).This possibility seems to destroy much of the need to postulate a role for T cell suppressors (Tregs) in cancer, but the exposure of effector T cells to antigen may convert them into Tregs (Tregs do exist).

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, University of Washington School of Medicine, Seattle 98118, USA. prehn@u.washington.edu

ABSTRACT
There exists a very large literature suggesting that T cells come in a variety of species and that without the action of Tregs tumors would seldom survive inhibition by T cell effectors. We believe that much of the evidence supporting the role of Tregs in cancer is compatible with a perhaps simpler hypothesis based upon the demonstration that that small quantities of effector T cells tend to stimulate tumors while larger quantities of seemingly the same cells are inhibitory (an hormesis-like effect). This possibility seems to destroy much of the need to postulate a role for T cell suppressors (Tregs) in cancer, but the exposure of effector T cells to antigen may convert them into Tregs (Tregs do exist). Furthermore, many other data suggest the possibility that immune inhibition of cancer could be a laboratory artifact seldom if ever seen in unmodified nature.

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Possible scheme for the mechanism of immune-stimulation of tumor growth.
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Figure 2: Possible scheme for the mechanism of immune-stimulation of tumor growth.

Mentions: The facts suggest that a tumor inhibiting immunity is probably a laboratory artifact seldom, if ever, to be found in unaided nature. However, if one believes in the Sonnenschein thesis (which we do), growth and mutiplication are the default conditions of all living cells [26]. Therefore any cell, including a cancerous cell, that fails to grow is being inhibited by some environmental influence. Untransplanted cancers are usually and perhaps continuously stimulated rather than inhibited by the “immune” reaction engendered by them The mechanism of the stimulation could well be an interference by immune T cells of the tumor inhibition provided by the surrounding normal tissue environment [27] (see Figure 2).


Tumor inhibitory T cell immunity may be largely a transplantation artifact not necessarily dependent upon a lack of Tregs.

Prehn RT, Prehn LM - Theor Biol Med Model (2013)

Possible scheme for the mechanism of immune-stimulation of tumor growth.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750814&req=5

Figure 2: Possible scheme for the mechanism of immune-stimulation of tumor growth.
Mentions: The facts suggest that a tumor inhibiting immunity is probably a laboratory artifact seldom, if ever, to be found in unaided nature. However, if one believes in the Sonnenschein thesis (which we do), growth and mutiplication are the default conditions of all living cells [26]. Therefore any cell, including a cancerous cell, that fails to grow is being inhibited by some environmental influence. Untransplanted cancers are usually and perhaps continuously stimulated rather than inhibited by the “immune” reaction engendered by them The mechanism of the stimulation could well be an interference by immune T cells of the tumor inhibition provided by the surrounding normal tissue environment [27] (see Figure 2).

Bottom Line: There exists a very large literature suggesting that T cells come in a variety of species and that without the action of Tregs tumors would seldom survive inhibition by T cell effectors.We believe that much of the evidence supporting the role of Tregs in cancer is compatible with a perhaps simpler hypothesis based upon the demonstration that that small quantities of effector T cells tend to stimulate tumors while larger quantities of seemingly the same cells are inhibitory (an hormesis-like effect).This possibility seems to destroy much of the need to postulate a role for T cell suppressors (Tregs) in cancer, but the exposure of effector T cells to antigen may convert them into Tregs (Tregs do exist).

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, University of Washington School of Medicine, Seattle 98118, USA. prehn@u.washington.edu

ABSTRACT
There exists a very large literature suggesting that T cells come in a variety of species and that without the action of Tregs tumors would seldom survive inhibition by T cell effectors. We believe that much of the evidence supporting the role of Tregs in cancer is compatible with a perhaps simpler hypothesis based upon the demonstration that that small quantities of effector T cells tend to stimulate tumors while larger quantities of seemingly the same cells are inhibitory (an hormesis-like effect). This possibility seems to destroy much of the need to postulate a role for T cell suppressors (Tregs) in cancer, but the exposure of effector T cells to antigen may convert them into Tregs (Tregs do exist). Furthermore, many other data suggest the possibility that immune inhibition of cancer could be a laboratory artifact seldom if ever seen in unmodified nature.

Show MeSH
Related in: MedlinePlus