LOSS OF SUPPRESSOR FUNCTION AS A CAUSE OF LYMPHOID MALIGNANCY

M. Eric Gershwin, AlfredD Steinberg

Research output: Contribution to journalArticle

49 Citations (Scopus)

Abstract

Different lymphoid-cell populations have been shown to interact in various immunological responses. A lymphoid-cell population that is capable of suppressing humoral and cellular immunity has been demonstrated. It is proposed that suppressor cells normally regulate continued lymphoid hyperplasia in response to various stimuli. In the absence of suppressor function, unregulated proliferation would ultimately lead to lymphoreticular malignancy. According to this mechanism, restoration of suppressor cells might prevent the development of lymphoreticular malignancies.

Original languageEnglish (US)
Pages (from-to)1174-1176
Number of pages3
JournalThe Lancet
Volume302
Issue number7839
DOIs
StatePublished - Nov 24 1973
Externally publishedYes

Fingerprint

Lymphocytes
Humoral Immunity
Cellular Immunity
Population
Hyperplasia
Neoplasms

ASJC Scopus subject areas

  • Medicine(all)

Cite this

LOSS OF SUPPRESSOR FUNCTION AS A CAUSE OF LYMPHOID MALIGNANCY. / Gershwin, M. Eric; Steinberg, AlfredD.

In: The Lancet, Vol. 302, No. 7839, 24.11.1973, p. 1174-1176.

Research output: Contribution to journalArticle

Gershwin, M. Eric ; Steinberg, AlfredD. / LOSS OF SUPPRESSOR FUNCTION AS A CAUSE OF LYMPHOID MALIGNANCY. In: The Lancet. 1973 ; Vol. 302, No. 7839. pp. 1174-1176.
@article{3fb6bbe1f4a24e59a26ed1ba26f4e469,
title = "LOSS OF SUPPRESSOR FUNCTION AS A CAUSE OF LYMPHOID MALIGNANCY",
abstract = "Different lymphoid-cell populations have been shown to interact in various immunological responses. A lymphoid-cell population that is capable of suppressing humoral and cellular immunity has been demonstrated. It is proposed that suppressor cells normally regulate continued lymphoid hyperplasia in response to various stimuli. In the absence of suppressor function, unregulated proliferation would ultimately lead to lymphoreticular malignancy. According to this mechanism, restoration of suppressor cells might prevent the development of lymphoreticular malignancies.",
author = "Gershwin, {M. Eric} and AlfredD Steinberg",
year = "1973",
month = "11",
day = "24",
doi = "10.1016/S0140-6736(73)92940-1",
language = "English (US)",
volume = "302",
pages = "1174--1176",
journal = "The Lancet",
issn = "0140-6736",
publisher = "Elsevier Limited",
number = "7839",

}

TY - JOUR

T1 - LOSS OF SUPPRESSOR FUNCTION AS A CAUSE OF LYMPHOID MALIGNANCY

AU - Gershwin, M. Eric

AU - Steinberg, AlfredD

PY - 1973/11/24

Y1 - 1973/11/24

N2 - Different lymphoid-cell populations have been shown to interact in various immunological responses. A lymphoid-cell population that is capable of suppressing humoral and cellular immunity has been demonstrated. It is proposed that suppressor cells normally regulate continued lymphoid hyperplasia in response to various stimuli. In the absence of suppressor function, unregulated proliferation would ultimately lead to lymphoreticular malignancy. According to this mechanism, restoration of suppressor cells might prevent the development of lymphoreticular malignancies.

AB - Different lymphoid-cell populations have been shown to interact in various immunological responses. A lymphoid-cell population that is capable of suppressing humoral and cellular immunity has been demonstrated. It is proposed that suppressor cells normally regulate continued lymphoid hyperplasia in response to various stimuli. In the absence of suppressor function, unregulated proliferation would ultimately lead to lymphoreticular malignancy. According to this mechanism, restoration of suppressor cells might prevent the development of lymphoreticular malignancies.

UR - http://www.scopus.com/inward/record.url?scp=0015897871&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0015897871&partnerID=8YFLogxK

U2 - 10.1016/S0140-6736(73)92940-1

DO - 10.1016/S0140-6736(73)92940-1

M3 - Article

C2 - 4127550

AN - SCOPUS:0015897871

VL - 302

SP - 1174

EP - 1176

JO - The Lancet

JF - The Lancet

SN - 0140-6736

IS - 7839

ER -