Document Detail


Late pregnancy suppresses relapses in experimental autoimmune encephalomyelitis: evidence for a suppressive pregnancy-related serum factor.
MedLine Citation:
PMID:  12097417     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Annette Langer-Gould; Hideki Garren; Amy Slansky; Pedro J Ruiz; Lawrence Steinman
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  169     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2002 Jul 
Date Detail:
Created Date:  2002-07-04     Completed Date:  2002-08-28     Revised Date:  2011-08-26    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1084-91     Citation Subset:  AIM; IM    
Affiliation:
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA. annette1@stanford.edu
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MeSH Terms
Descriptor/Qualifier:
Adoptive Transfer
Amino Acid Sequence
Animals
Autoantigens / adverse effects,  pharmacology
Cell Movement / immunology
Cytokines / biosynthesis
Disease Susceptibility / immunology
Dysgammaglobulinemia / blood,  immunology
Encephalomyelitis, Autoimmune, Experimental / blood,  immunology*,  pathology,  prevention & control*
Female
Immunoglobulin G / biosynthesis,  blood
Interleukin-2 / antagonists & inhibitors,  biosynthesis
Lymph Nodes / cytology,  immunology,  transplantation
Lymphocyte Activation / immunology
Male
Mice
Mice, Inbred Strains
Molecular Sequence Data
Myelin Proteolipid Protein / administration & dosage,  immunology
Peptide Fragments / administration & dosage,  immunology
Pregnancy
Pregnancy Complications / blood,  immunology*,  pathology,  prevention & control*
Pregnancy, Animal / blood,  immunology*
Recurrence / prevention & control
Suppressor Factors, Immunologic / blood,  physiology*
Th1 Cells / immunology,  metabolism
Transforming Growth Factor beta / blood
Grant Support
ID/Acronym/Agency:
1K08AI01494-01/AI/NIAID NIH HHS; AI07290-15/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Autoantigens; 0/Cytokines; 0/Immunoglobulin G; 0/Interleukin-2; 0/Myelin Proteolipid Protein; 0/Peptide Fragments; 0/Suppressor Factors, Immunologic; 0/Transforming Growth Factor beta; 0/myelin proteolipid protein (139-151)

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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