Gangliosides GD1b, GT1b, and GQ1b enhance IL-2 and IFN-gamma production and suppress IL-4 and IL-5 production in phytohemagglutinin-stimulated human T cells

J Immunol. 2001 Jan 1;166(1):72-80. doi: 10.4049/jimmunol.166.1.72.

Abstract

Gangliosides are sialic acid-containing glycolipids. We studied the in vitro effects of gangliosides on Th1 and Th2 cytokine production in PHA-stimulated human T cells. Gangliosides GD1b, GT1b, and GQ1b (each 100 nM) enhanced PHA-induced IL-2 secretion of peripheral blood T cells approximately 4-fold and enhanced that of IFN-gamma 3- to 4-fold compared with controls. These gangliosides decreased PHA-induced IL-4 secretion by 50-53% and that of IL-5 by 53-63% compared with controls, respectively. The other gangliosides did not alter the secretion of Th1 or Th2 cytokines. RT-PCR showed that GD1b, GT1b, and GQ1b enhanced PHA-induced IL-2 and IFN-gamma transcription and suppressed that of IL-4 and IL-5. Transient transfection assays of Jurkat T cells showed that GD1b, GT1b, and GQ1b enhanced PHA-induced IL-2 and IFN-gamma promoter activities but suppressed those of IL-4 and IL-5. The cAMP analogue dibutyryl cAMP and the cAMP-elevating agents forskolin and 3-isobutyl-1-methylxanthine each reversed GD1b-, GT1b-, and GQ1b-induced stimulation of IL-2 and IFN-gamma production and inhibition of IL-4 and IL-5 production at the levels of proteins, transcription, and promoter activities. GD1b, GT1b, and GQ1b suppressed PHA-induced increase in cAMP level in T cells. These gangliosides suppressed PHA-stimulated adenylate cyclase activity in T cells. These results suggest that GD1b, GT1b, and GQ1b may enhance Th1 cytokine production while suppressing Th2 production by inhibiting adenylate cyclase activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenylyl Cyclase Inhibitors
  • Adenylyl Cyclases / metabolism
  • Adjuvants, Immunologic / antagonists & inhibitors
  • Adjuvants, Immunologic / pharmacology
  • Adult
  • Cyclic AMP / metabolism
  • Cyclic AMP / physiology
  • Cyclic AMP-Dependent Protein Kinase Type II
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Enzyme Activation / drug effects
  • Enzyme Activation / immunology
  • Female
  • Gangliosides / antagonists & inhibitors
  • Gangliosides / pharmacology*
  • Humans
  • Immunosuppressive Agents / antagonists & inhibitors
  • Immunosuppressive Agents / pharmacology
  • Interferon-gamma / biosynthesis*
  • Interleukin-2 / biosynthesis*
  • Interleukin-4 / antagonists & inhibitors*
  • Interleukin-4 / biosynthesis
  • Interleukin-4 / metabolism
  • Interleukin-5 / antagonists & inhibitors*
  • Interleukin-5 / biosynthesis
  • Interleukin-5 / metabolism
  • Jurkat Cells
  • Lymphocyte Activation* / drug effects
  • Male
  • Middle Aged
  • Phosphoric Diester Hydrolases / metabolism
  • Phytohemagglutinins / antagonists & inhibitors
  • Phytohemagglutinins / pharmacology*
  • Promoter Regions, Genetic / drug effects
  • Promoter Regions, Genetic / genetics
  • Promoter Regions, Genetic / immunology
  • RNA, Messenger / antagonists & inhibitors
  • RNA, Messenger / biosynthesis
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / enzymology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*
  • Th1 Cells / drug effects
  • Th1 Cells / metabolism
  • Th2 Cells / drug effects
  • Th2 Cells / metabolism

Substances

  • Adenylyl Cyclase Inhibitors
  • Adjuvants, Immunologic
  • Gangliosides
  • Immunosuppressive Agents
  • Interleukin-2
  • Interleukin-5
  • Phytohemagglutinins
  • RNA, Messenger
  • ganglioside, GD1b
  • Interleukin-4
  • trisialoganglioside GT1
  • GQ1b ganglioside
  • Interferon-gamma
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinase Type II
  • Cyclic AMP-Dependent Protein Kinases
  • Phosphoric Diester Hydrolases
  • Adenylyl Cyclases