Helper factor(s) generated by tumor-immune rats for lymphoproliferative responses to syngeneic tumor cells

Michael A. Hollingsworth; Donald L. Evans

doi:10.1093/jnci/72.6.1357

Helper factor(s) generated by tumor-immune rats for lymphoproliferative responses to syngeneic tumor cells

Michael A. Hollingsworth, Donald L. Evans

Research output: Contribution to journal › Article › peer-review

Abstract

New Zealand Black (NBR) rats that are innately immune to challenge with a syngeneic 3-methylcholanthrene [(MCA) CAS: 56-49-5]-induced fibrosarcoma have spleen cells that produce helper effects for in vitro lymphoproliferative responses in the presence of individual MCA-induced fibrosarcoma cells. Spleen cells from MCA-induced fibrosarcoma progressor rats (which lack innate tumor immunity) do not produce demonstrable helper activity. Supernatants from 48-hour cocultures of spleen cells from tumor-immune (TI) rats and syngeneic MCA-induced fibrosarcoma cells replaced the spleen cell helper activity. Comparable spleen cell supernatants from tumor progressor rats or unchallenged rats (controls) as well as supernatants from MCA-induced fibrosarcoma cells cultured alone did not produce any helper factor activity. Supernatants from TI rat spleen cells following inoculation with MCA-induced fibrosarcoma cells did not affect lymphoproliferative responses of NBR spleen cells induced by concanavalin A or alloantigens. The supernatants also did not contain detectable interleukin 2 activity as determined with the use of the thymocyte costimulator assay. These data indicate that the production of soluble helper factors by TI rat spleen cells may be involved in the augmentation of a protective host antitumor response.

Original language	English (US)
Pages (from-to)	1357-1363
Number of pages	7
Journal	Journal of the National Cancer Institute
Volume	72
Issue number	6
DOIs	https://doi.org/10.1093/jnci/72.6.1357
State	Published - Jun 1984
Externally published	Yes

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1093/jnci/72.6.1357

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@article{d99a7a05f6d5429b981d7a809b4a074e,

title = "Helper factor(s) generated by tumor-immune rats for lymphoproliferative responses to syngeneic tumor cells",

abstract = "New Zealand Black (NBR) rats that are innately immune to challenge with a syngeneic 3-methylcholanthrene [(MCA) CAS: 56-49-5]-induced fibrosarcoma have spleen cells that produce helper effects for in vitro lymphoproliferative responses in the presence of individual MCA-induced fibrosarcoma cells. Spleen cells from MCA-induced fibrosarcoma progressor rats (which lack innate tumor immunity) do not produce demonstrable helper activity. Supernatants from 48-hour cocultures of spleen cells from tumor-immune (TI) rats and syngeneic MCA-induced fibrosarcoma cells replaced the spleen cell helper activity. Comparable spleen cell supernatants from tumor progressor rats or unchallenged rats (controls) as well as supernatants from MCA-induced fibrosarcoma cells cultured alone did not produce any helper factor activity. Supernatants from TI rat spleen cells following inoculation with MCA-induced fibrosarcoma cells did not affect lymphoproliferative responses of NBR spleen cells induced by concanavalin A or alloantigens. The supernatants also did not contain detectable interleukin 2 activity as determined with the use of the thymocyte costimulator assay. These data indicate that the production of soluble helper factors by TI rat spleen cells may be involved in the augmentation of a protective host antitumor response.",

author = "Hollingsworth, {Michael A.} and Evans, {Donald L.}",

note = "Funding Information: I Received April 14, 1983; revised January 9, 1984; accepted January 27, 1984. 2 Supported in part by Public Health Service grant 5T32CA-09422 from the National Cancer Institute, by American Cancer Society grant IM 220, and by the Gaston County Cancer Society and the Edward and Ruth Diehl Foundation. 3 Portions of this article have been presented previously in the doctoral dissertation of M. A. Hollingsworth. 4 Department of Microbiology and Immunology, Bowman Gray School of Medicine, Winston-Salem, N.C. 27103. 5 Present address: Division of Immunology, Duke University, Box 3839, Durham, N.C. 27706. 6 Department of Medical Microbiology, College of Veterinary Medicine, University of Georgia, Athens, Ga. 30602.",

year = "1984",

month = jun,

doi = "10.1093/jnci/72.6.1357",

language = "English (US)",

volume = "72",

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journal = "Journal of the National Cancer Institute",

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T1 - Helper factor(s) generated by tumor-immune rats for lymphoproliferative responses to syngeneic tumor cells

AU - Hollingsworth, Michael A.

AU - Evans, Donald L.

N1 - Funding Information: I Received April 14, 1983; revised January 9, 1984; accepted January 27, 1984. 2 Supported in part by Public Health Service grant 5T32CA-09422 from the National Cancer Institute, by American Cancer Society grant IM 220, and by the Gaston County Cancer Society and the Edward and Ruth Diehl Foundation. 3 Portions of this article have been presented previously in the doctoral dissertation of M. A. Hollingsworth. 4 Department of Microbiology and Immunology, Bowman Gray School of Medicine, Winston-Salem, N.C. 27103. 5 Present address: Division of Immunology, Duke University, Box 3839, Durham, N.C. 27706. 6 Department of Medical Microbiology, College of Veterinary Medicine, University of Georgia, Athens, Ga. 30602.

PY - 1984/6

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N2 - New Zealand Black (NBR) rats that are innately immune to challenge with a syngeneic 3-methylcholanthrene [(MCA) CAS: 56-49-5]-induced fibrosarcoma have spleen cells that produce helper effects for in vitro lymphoproliferative responses in the presence of individual MCA-induced fibrosarcoma cells. Spleen cells from MCA-induced fibrosarcoma progressor rats (which lack innate tumor immunity) do not produce demonstrable helper activity. Supernatants from 48-hour cocultures of spleen cells from tumor-immune (TI) rats and syngeneic MCA-induced fibrosarcoma cells replaced the spleen cell helper activity. Comparable spleen cell supernatants from tumor progressor rats or unchallenged rats (controls) as well as supernatants from MCA-induced fibrosarcoma cells cultured alone did not produce any helper factor activity. Supernatants from TI rat spleen cells following inoculation with MCA-induced fibrosarcoma cells did not affect lymphoproliferative responses of NBR spleen cells induced by concanavalin A or alloantigens. The supernatants also did not contain detectable interleukin 2 activity as determined with the use of the thymocyte costimulator assay. These data indicate that the production of soluble helper factors by TI rat spleen cells may be involved in the augmentation of a protective host antitumor response.

AB - New Zealand Black (NBR) rats that are innately immune to challenge with a syngeneic 3-methylcholanthrene [(MCA) CAS: 56-49-5]-induced fibrosarcoma have spleen cells that produce helper effects for in vitro lymphoproliferative responses in the presence of individual MCA-induced fibrosarcoma cells. Spleen cells from MCA-induced fibrosarcoma progressor rats (which lack innate tumor immunity) do not produce demonstrable helper activity. Supernatants from 48-hour cocultures of spleen cells from tumor-immune (TI) rats and syngeneic MCA-induced fibrosarcoma cells replaced the spleen cell helper activity. Comparable spleen cell supernatants from tumor progressor rats or unchallenged rats (controls) as well as supernatants from MCA-induced fibrosarcoma cells cultured alone did not produce any helper factor activity. Supernatants from TI rat spleen cells following inoculation with MCA-induced fibrosarcoma cells did not affect lymphoproliferative responses of NBR spleen cells induced by concanavalin A or alloantigens. The supernatants also did not contain detectable interleukin 2 activity as determined with the use of the thymocyte costimulator assay. These data indicate that the production of soluble helper factors by TI rat spleen cells may be involved in the augmentation of a protective host antitumor response.

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Helper factor(s) generated by tumor-immune rats for lymphoproliferative responses to syngeneic tumor cells

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