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Title: Influence of tunicamycin, sialidase, and cholera toxin on gangliosides and T-lymphocyte responses to interleukin 2

Abstract

The authors have shown that gangliosides inhibit interleukin 2 (IL 2)-dependent proliferation of murine T cells. Tunicamycin (TM), sialidase, and cholera toxin-..beta.. subunit (..beta..-CT) are known modulators of cell surface glycoconjugates. To test the possible role of endogenous gangliosides in T cell responses to IL-2, the effect of these agents on ganglioside expression and cell proliferation was studied. Gangliosides were labelled for 24 hrs with /sup 3/H-glucosamine/galactose in the presence of IL-2 and purified sialidase, TM or ..beta..-CT. Gangliosides were isolated and the species separated by TLC. Alternatively, proliferation was assayed by /sup 3/H-thymidine uptake after 48 hrs culture. TM treatment at a concentration (10 ..mu..g/ml) that completely inhibited proliferation resulted in a 86% reduction of incorporation of saccharide precursors into gangliosides compared to a 50% reduction into proteins. Sialidase treatment (0.1 IU/ml) resulted in a 70% inhibition of proliferation and 30% reduction of radiolabel into gangliosides, of which 3 species were specifically reduced. ..beta..-CT, which binds to GM/sub 1/ and to a lesser extent GD/sub 1a/, caused a 50% reduction in proliferation response at 35 units/ml. The results support the hypothesis that gangliosides are involved in IL-2-dependent proliferation.

Authors:
; ;
Publication Date:
Research Org.:
George Washington Univ. School of Medicine and Health Sciences, Washington, DC
OSTI Identifier:
7245125
Report Number(s):
CONF-8606151-
Journal ID: CODEN: FEPRA; TRN: 86-039297
Resource Type:
Conference
Journal Name:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
Additional Journal Information:
Journal Volume: 45:6; Conference: 76. annual meeting of the Federation of American Society for Experimental Biology, Washington, DC, USA, 8 Jun 1986
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; 59 BASIC BIOLOGICAL SCIENCES; ANTIBIOTICS; BIOLOGICAL EFFECTS; GANGLIOSIDES; LABELLING; LYMPHOCYTES; CELL PROLIFERATION; LYMPHOKINES; TOXINS; GALACTOSE; GLUCOSAMINE; THIN-LAYER CHROMATOGRAPHY; THYMIDINE; TRACER TECHNIQUES; TRITIUM COMPOUNDS; ALDEHYDES; AMINES; ANIMAL CELLS; ANTI-INFECTIVE AGENTS; ANTIGENS; AZINES; BIOLOGICAL MATERIALS; BLOOD; BLOOD CELLS; BODY FLUIDS; CARBOHYDRATES; CHROMATOGRAPHY; CONNECTIVE TISSUE CELLS; DRUGS; GROWTH FACTORS; HETEROCYCLIC COMPOUNDS; HEXOSAMINES; HEXOSES; ISOTOPE APPLICATIONS; LABELLED COMPOUNDS; LEUKOCYTES; LIPIDS; MATERIALS; MITOGENS; MONOSACCHARIDES; NUCLEOSIDES; NUCLEOTIDES; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; PROTEINS; PYRIMIDINES; RIBOSIDES; SACCHARIDES; SEPARATION PROCESSES; SOMATIC CELLS; TOXIC MATERIALS; 560300* - Chemicals Metabolism & Toxicology; 550201 - Biochemistry- Tracer Techniques

Citation Formats

Semmes, O J, Bailey, J M, and Merritt, W D. Influence of tunicamycin, sialidase, and cholera toxin on gangliosides and T-lymphocyte responses to interleukin 2. United States: N. p., 1986. Web.
Semmes, O J, Bailey, J M, & Merritt, W D. Influence of tunicamycin, sialidase, and cholera toxin on gangliosides and T-lymphocyte responses to interleukin 2. United States.
Semmes, O J, Bailey, J M, and Merritt, W D. 1986. "Influence of tunicamycin, sialidase, and cholera toxin on gangliosides and T-lymphocyte responses to interleukin 2". United States.
@article{osti_7245125,
title = {Influence of tunicamycin, sialidase, and cholera toxin on gangliosides and T-lymphocyte responses to interleukin 2},
author = {Semmes, O J and Bailey, J M and Merritt, W D},
abstractNote = {The authors have shown that gangliosides inhibit interleukin 2 (IL 2)-dependent proliferation of murine T cells. Tunicamycin (TM), sialidase, and cholera toxin-..beta.. subunit (..beta..-CT) are known modulators of cell surface glycoconjugates. To test the possible role of endogenous gangliosides in T cell responses to IL-2, the effect of these agents on ganglioside expression and cell proliferation was studied. Gangliosides were labelled for 24 hrs with /sup 3/H-glucosamine/galactose in the presence of IL-2 and purified sialidase, TM or ..beta..-CT. Gangliosides were isolated and the species separated by TLC. Alternatively, proliferation was assayed by /sup 3/H-thymidine uptake after 48 hrs culture. TM treatment at a concentration (10 ..mu..g/ml) that completely inhibited proliferation resulted in a 86% reduction of incorporation of saccharide precursors into gangliosides compared to a 50% reduction into proteins. Sialidase treatment (0.1 IU/ml) resulted in a 70% inhibition of proliferation and 30% reduction of radiolabel into gangliosides, of which 3 species were specifically reduced. ..beta..-CT, which binds to GM/sub 1/ and to a lesser extent GD/sub 1a/, caused a 50% reduction in proliferation response at 35 units/ml. The results support the hypothesis that gangliosides are involved in IL-2-dependent proliferation.},
doi = {},
url = {https://www.osti.gov/biblio/7245125}, journal = {Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)},
number = ,
volume = 45:6,
place = {United States},
year = {Thu May 01 00:00:00 EDT 1986},
month = {Thu May 01 00:00:00 EDT 1986}
}

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