title: Late pregnancy suppresses relapses in experimental autoimmune encephalomyelitis: evidence for a suppressive pregnancy-related serum factor.
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.
authors.affiliation: Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA. annette1@stanford.edu
authors.forename: Annette
authors.initials: A
authors.lastname: Langer-Gould
authors.forename: Hideki
authors.initials: H
authors.lastname: Garren
authors.forename: Amy
authors.initials: A
authors.lastname: Slansky
authors.forename: Pedro J
authors.initials: PJ
authors.lastname: Ruiz
authors.forename: Lawrence
authors.initials: L
authors.lastname: Steinman
mesh_terms: D019264:Adoptive Transfer; D000595:Amino Acid Sequence; D000818:Animals; D001324:Autoantigens / Q000009:adverse effects / Q000494:pharmacology; D002465:Cell Movement / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D004198:Disease Susceptibility / Q000276:immunology; D004406:Dysgammaglobulinemia / Q000097:blood / Q000276:immunology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control*; D005260:Female; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000097:blood; D007376:Interleukin-2 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology / Q000637:transplantation; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008969:Molecular Sequence Data; D018991:Myelin Proteolipid Protein / Q000008:administration & dosage / Q000276:immunology; D010446:Peptide Fragments / Q000008:administration & dosage / Q000276:immunology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control*; D011270:Pregnancy, Animal / Q000097:blood / Q000276:immunology*; D055502:Secondary Prevention; D013491:Suppressor Factors, Immunologic / Q000097:blood / Q000502:physiology*; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000097:blood
chemical_list: D001324:Autoantigens; D016207:Cytokines; D007074:Immunoglobulin G; D007376:Interleukin-2; D018991:Myelin Proteolipid Protein; D010446:Peptide Fragments; D013491:Suppressor Factors, Immunologic; D016212:Transforming Growth Factor beta; C435023:myelin proteolipid protein (139-151)