Abrogation of proliferation and generation of cytotoxic T cells in human mixed lymphocyte culture reactions by modification of the cell surface with mitogenic oxidizing agents

Manikkam Suthanthiran, Albert L. Rubin, Abraham Novogrodsky, Kurt H. Stenzel

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Multiple lectins with specificity for cell surface glycoproteins inhibit cellular and humoral immune responses and induce transplantation tolerance. Because cell surface glycoproteins play a significant role in various immune events involving cell to cell interactions and because the mixed lymphocyte culture (MLC) reaction is a prototype of immune phenomenon involving cell to cell interactions as well as an in vitro analogue of graft-destructive immune events, the effect of modification of the cell surface with oxidizing mitogens was investigated. Treatment of responder or stimulator cells with neuraminidase and galactose oxidase (NAGO) or with sodium periodate (Equation found) resulted in marked suppression of alloantigen-induced proliferation and in vitro generation of primary cytotoxic T cells (CTLs) in human MLCs. A prominent coupling of mitogen-induced proliferation to abrogation of MLC was consistently observed with modification of stimulator or responder cell surface with either NAGO or (Equation found). The possibility that destruction of receptor sites and/or stimulatory units was responsible for the suppression of MLCs was excluded by restoring both proliferation and generation of primary CTLs by reduction of mitogen-oxidized cell surfaces with sodium borohydride. The ability of polyclonal activators to inhibit antigen-specific responses might be useful in abrogating unfavorable alloimmune responses.

Original languageEnglish
Pages (from-to)209-214
Number of pages6
JournalTransplantation
Volume34
Issue number4
DOIs
Publication statusPublished - 1 Jan 1982
Externally publishedYes

Fingerprint

Mixed Lymphocyte Culture Test
Oxidants
Galactose Oxidase
Mitogens
T-Lymphocytes
Membrane Glycoproteins
Neuraminidase
Cell Communication
Transplantation Tolerance
Isoantigens
Humoral Immunity
Lectins
Cellular Immunity
Lymphocytes
Transplants
Antigens
In Vitro Techniques
Therapeutics

ASJC Scopus subject areas

  • Transplantation

Cite this

Abrogation of proliferation and generation of cytotoxic T cells in human mixed lymphocyte culture reactions by modification of the cell surface with mitogenic oxidizing agents. / Suthanthiran, Manikkam; Rubin, Albert L.; Novogrodsky, Abraham; Stenzel, Kurt H.

In: Transplantation, Vol. 34, No. 4, 01.01.1982, p. 209-214.

Research output: Contribution to journalArticle

@article{891038423897453ab7fb6b51960b5e91,
title = "Abrogation of proliferation and generation of cytotoxic T cells in human mixed lymphocyte culture reactions by modification of the cell surface with mitogenic oxidizing agents",
abstract = "Multiple lectins with specificity for cell surface glycoproteins inhibit cellular and humoral immune responses and induce transplantation tolerance. Because cell surface glycoproteins play a significant role in various immune events involving cell to cell interactions and because the mixed lymphocyte culture (MLC) reaction is a prototype of immune phenomenon involving cell to cell interactions as well as an in vitro analogue of graft-destructive immune events, the effect of modification of the cell surface with oxidizing mitogens was investigated. Treatment of responder or stimulator cells with neuraminidase and galactose oxidase (NAGO) or with sodium periodate (Equation found) resulted in marked suppression of alloantigen-induced proliferation and in vitro generation of primary cytotoxic T cells (CTLs) in human MLCs. A prominent coupling of mitogen-induced proliferation to abrogation of MLC was consistently observed with modification of stimulator or responder cell surface with either NAGO or (Equation found). The possibility that destruction of receptor sites and/or stimulatory units was responsible for the suppression of MLCs was excluded by restoring both proliferation and generation of primary CTLs by reduction of mitogen-oxidized cell surfaces with sodium borohydride. The ability of polyclonal activators to inhibit antigen-specific responses might be useful in abrogating unfavorable alloimmune responses.",
author = "Manikkam Suthanthiran and Rubin, {Albert L.} and Abraham Novogrodsky and Stenzel, {Kurt H.}",
year = "1982",
month = "1",
day = "1",
doi = "10.1097/00007890-198210000-00010",
language = "English",
volume = "34",
pages = "209--214",
journal = "Transplantation",
issn = "0041-1337",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Abrogation of proliferation and generation of cytotoxic T cells in human mixed lymphocyte culture reactions by modification of the cell surface with mitogenic oxidizing agents

AU - Suthanthiran, Manikkam

AU - Rubin, Albert L.

AU - Novogrodsky, Abraham

AU - Stenzel, Kurt H.

PY - 1982/1/1

Y1 - 1982/1/1

N2 - Multiple lectins with specificity for cell surface glycoproteins inhibit cellular and humoral immune responses and induce transplantation tolerance. Because cell surface glycoproteins play a significant role in various immune events involving cell to cell interactions and because the mixed lymphocyte culture (MLC) reaction is a prototype of immune phenomenon involving cell to cell interactions as well as an in vitro analogue of graft-destructive immune events, the effect of modification of the cell surface with oxidizing mitogens was investigated. Treatment of responder or stimulator cells with neuraminidase and galactose oxidase (NAGO) or with sodium periodate (Equation found) resulted in marked suppression of alloantigen-induced proliferation and in vitro generation of primary cytotoxic T cells (CTLs) in human MLCs. A prominent coupling of mitogen-induced proliferation to abrogation of MLC was consistently observed with modification of stimulator or responder cell surface with either NAGO or (Equation found). The possibility that destruction of receptor sites and/or stimulatory units was responsible for the suppression of MLCs was excluded by restoring both proliferation and generation of primary CTLs by reduction of mitogen-oxidized cell surfaces with sodium borohydride. The ability of polyclonal activators to inhibit antigen-specific responses might be useful in abrogating unfavorable alloimmune responses.

AB - Multiple lectins with specificity for cell surface glycoproteins inhibit cellular and humoral immune responses and induce transplantation tolerance. Because cell surface glycoproteins play a significant role in various immune events involving cell to cell interactions and because the mixed lymphocyte culture (MLC) reaction is a prototype of immune phenomenon involving cell to cell interactions as well as an in vitro analogue of graft-destructive immune events, the effect of modification of the cell surface with oxidizing mitogens was investigated. Treatment of responder or stimulator cells with neuraminidase and galactose oxidase (NAGO) or with sodium periodate (Equation found) resulted in marked suppression of alloantigen-induced proliferation and in vitro generation of primary cytotoxic T cells (CTLs) in human MLCs. A prominent coupling of mitogen-induced proliferation to abrogation of MLC was consistently observed with modification of stimulator or responder cell surface with either NAGO or (Equation found). The possibility that destruction of receptor sites and/or stimulatory units was responsible for the suppression of MLCs was excluded by restoring both proliferation and generation of primary CTLs by reduction of mitogen-oxidized cell surfaces with sodium borohydride. The ability of polyclonal activators to inhibit antigen-specific responses might be useful in abrogating unfavorable alloimmune responses.

UR - http://www.scopus.com/inward/record.url?scp=0019921549&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019921549&partnerID=8YFLogxK

U2 - 10.1097/00007890-198210000-00010

DO - 10.1097/00007890-198210000-00010

M3 - Article

VL - 34

SP - 209

EP - 214

JO - Transplantation

JF - Transplantation

SN - 0041-1337

IS - 4

ER -