Late pregnancy suppresses relapses in experimental autoimmune encephalomyelitis: evidence for a suppressive pregnancy-related serum factor

J Immunol. 2002 Jul 15;169(2):1084-91. doi: 10.4049/jimmunol.169.2.1084.

Abstract

Women with multiple sclerosis have significantly diminished disease activity during pregnancy. The purpose of our study was to identify the underlying mechanism for the diminished disease activity. We found that during the period of late pregnancy there is protection against paralysis, during both the induction and effector phases of relapsing experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. We did not find any changes in the cytokine secretion profiles or the proliferative activity of autoreactive T cells from mice induced during late pregnancy compared with virgin controls. In mice mated after disease onset, the inflammatory histologic lesions did not clear, despite marked clinical improvement during pregnancy. We found evidence for a serum factor present in late pregnancy that suppresses T cell activation. In the presence of sera taken from mice late in pregnancy, the proliferative response and IL-2 production of proteolipid protein p139-151-specific T cells were significantly diminished as compared with stimulation in the presence of normal mouse sera. In conclusion, serum from late pregnancy has the capacity to down-regulate T cell responses and might be associated with the amelioration of disease activity in experimental autoimmune encephalomyelitis.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adoptive Transfer
  • Amino Acid Sequence
  • Animals
  • Autoantigens / adverse effects
  • Autoantigens / pharmacology
  • Cell Movement / immunology
  • Cytokines / biosynthesis
  • Disease Susceptibility / immunology
  • Dysgammaglobulinemia / blood
  • Dysgammaglobulinemia / immunology
  • Encephalomyelitis, Autoimmune, Experimental / blood
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Encephalomyelitis, Autoimmune, Experimental / pathology
  • Encephalomyelitis, Autoimmune, Experimental / prevention & control*
  • Female
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin G / blood
  • Interleukin-2 / antagonists & inhibitors
  • Interleukin-2 / biosynthesis
  • Lymph Nodes / cytology
  • Lymph Nodes / immunology
  • Lymph Nodes / transplantation
  • Lymphocyte Activation / immunology
  • Male
  • Mice
  • Mice, Inbred Strains
  • Molecular Sequence Data
  • Myelin Proteolipid Protein / administration & dosage
  • Myelin Proteolipid Protein / immunology
  • Peptide Fragments / administration & dosage
  • Peptide Fragments / immunology
  • Pregnancy
  • Pregnancy Complications / blood
  • Pregnancy Complications / immunology*
  • Pregnancy Complications / pathology
  • Pregnancy Complications / prevention & control*
  • Pregnancy, Animal / blood
  • Pregnancy, Animal / immunology*
  • Secondary Prevention
  • Suppressor Factors, Immunologic / blood
  • Suppressor Factors, Immunologic / physiology*
  • Th1 Cells / immunology
  • Th1 Cells / metabolism
  • Transforming Growth Factor beta / blood

Substances

  • Autoantigens
  • Cytokines
  • Immunoglobulin G
  • Interleukin-2
  • Myelin Proteolipid Protein
  • Peptide Fragments
  • Suppressor Factors, Immunologic
  • Transforming Growth Factor beta
  • myelin proteolipid protein (139-151)