Cellular and Humoral immunity to Different Types of Human Neoplasms

Hellström, Ingegerd; Hellström, Karl Erik; Pierce, George E.; Yang, James P. S.

doi:10.1038/2201352a0

Cited by 354 publications

(53 citation statements)

References 16 publications

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“…Only the cells of one patient appeared to respond to substances present in homogenized tumor tissue. This effect is in marked contrast to the reports of Hellstrom et al (8,9), who have demonstrated responses of blood lymphocytes to tumor cells when assayed by a colony inhibition method. Our data is more consistent with the report of Savel (15) who found that approximately 12% of his patients had blood lymphocytes which responded to saline extracts of their autologous tumors.…”

contrasting

confidence: 83%

“…In man, syngeneic experiments are unlikely; skin testing has had limited investigation (13) and has suffered from the question of non-specific inflammation and the need to use soluble preparations of tumor. Tissue culture experiments have generally been too demanding for extensive investigation, although recently a (8,9,(14)(15)(16). A number of studies have recently demonstrated that peripheral blood lymphocyte transformation and proliferation in tissue culture, induced by antigens, is primarily a manifestation of cellular immunity (10,11).…”

mentioning

confidence: 99%

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In Vitro Responses of Lymphocytes from Cancer-Bearing Patients to Autochthonous Tumor Tissues

Hsu¹,

Cooperband²

1971

Experimental Biology and Medicine

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contrasting

confidence: 83%

mentioning

confidence: 99%

In Vitro Responses of Lymphocytes from Cancer-Bearing Patients to Autochthonous Tumor Tissues

Hsu¹,

Cooperband²

1971

Experimental Biology and Medicine

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“…For example, T-cell-mediated tumor rejection is rare despite that T lymphocytes can recognize antigens expressed by melanoma, and regardless of the massive influx of tumor antigen-specific T cells to the tumor site [42]. The coexistence of tumors and anti-tumor immune cells ("Hellstrom Paradox") [26,39,41,[43][44][45] has been a challenging problem for a long time.…”

Section: Abbreviationsmentioning

confidence: 99%

Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues

Lukashev

Ohta

Sitkovsky

2007

Cancer Metastasis Rev

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The evolutionarily selected tissue-protecting mechanisms are likely to be triggered by an event of universal significance for all surrounding cells. Such an event could be damage to blood vessels, which would result in local tissue hypoxia. It is now recognized that tissue hypoxia can initiate the tissue-protecting mechanism mediated by at least two different biochemical pathways. The central message of this review is that tumor cells are protected from immune damage in hypoxic and immunosuppressive tumor microenvironments due to the inactivation of anti-tumor T cells by the combined action of these two hypoxia-driven mechanisms. Firstly, tumor hypoxia-produced extracellular adenosine inhibits anti-tumor T cells via their G(s)-protein-coupled and cAMP-elevating A2A and A2B adenosine receptors (A2AR/A2BR). Levels of extracellular adenosine are increased in tumor microenvironments due to the changes in activities of enzymes involved in adenosine metabolism. Secondly, TCR-activated and/or tumor hypoxia-exposed anti-tumor T cells may be inhibited in tumor microenvironments by Hypoxia-inducible Factor 1alpha (HIF-1alpha) Hence, HIF-1alpha activity in T cells may contribute to the tumor-protecting immunosuppressive effects of tumor hypoxia. Here, we summarize the data that support the view that protection of hypoxic cancerous tissues from anti-tumor T cells is mediated by the same mechanism that protects normal tissues from the excessive collateral damage by overactive immune cells during acute inflammation.

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“…Attempts to demonstrate cellular hypersensitivity to these antigens using the technique of in-vitro blast transformation have not been successful (Lejtenyi, Freedman, and Gold, 1971) though Hellstrom, Hellstrom, Pierce, and Yang (1968) and Hellstrom, Sjogren, Warner, and Hellstrom (1971) were able to demonstrate direct lymphocyte cytotoxicity against tumour cells. The technique of leucocyte migration inhibition is a further test of cellular hypersensitivity to antigens (Rosenberg and David, 1970).…”

mentioning

confidence: 99%

Inhibition of leucocyte migration by tumour-associated antigens of the colon and rectum

Guillou¹,

Giles²

1973

Gut

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SUMMARY The test of leucocyte migration inhibition has been used to detect lymphocyte sensitization to tumour-associated antigens of the colon and rectum. The procedure for the isolation of antigens from colorectal adenocarcinomata and normal colonic mucosa is described. The Rolland, McGiven, and Hughes, 1971;Kleinman, Harwell, and Turner, 1971;Freed and Taylor, 1972). Attempts to demonstrate cellular hypersensitivity to these antigens using the technique of in-vitro blast transformation have not been successful (Lejtenyi, Freedman, and Gold, 1971)

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Cellular and Humoral immunity to Different Types of Human Neoplasms

Cited by 354 publications

References 16 publications

In Vitro Responses of Lymphocytes from Cancer-Bearing Patients to Autochthonous Tumor Tissues

In Vitro Responses of Lymphocytes from Cancer-Bearing Patients to Autochthonous Tumor Tissues

Hypoxia-dependent anti-inflammatory pathways in protection of cancerous tissues

Inhibition of leucocyte migration by tumour-associated antigens of the colon and rectum

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