Pregnancy and multiple sclerosis: feto-maternal immune cross talk and its implications for disease activity

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Pregnancy and multiple sclerosis: feto-maternal immune cross talk and its implications for disease activity. / Patas, Konstantinos; Engler, Jan Broder; Friese, Manuel A; Gold, Stefan M.

in: J REPROD IMMUNOL, Jahrgang 97, Nr. 1, 01.03.2013, S. 140-6.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{91d262497cb84a3199cad4150cad7b13,
title = "Pregnancy and multiple sclerosis: feto-maternal immune cross talk and its implications for disease activity",
abstract = "Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system of presumed autoimmune origin. Intriguingly, pregnancy in female MS patients is associated with a substantial decrease in relapse rate. However, post-partum the relapse rate increases in a rebounding fashion above the rate seen before pregnancy. Wide gaps remain in our understanding of the biological mechanisms underlying these pregnancy-related effects in MS patients. To date, most attempts to explain MS disease amelioration during pregnancy have focused on levels of circulating hormones with immunomodulatory properties such as estrogens and global shifts in systemic maternal immune cell composition. However, recent advances in our understanding of feto-maternal tolerance have provided evidence that fetal antigens directly interact with the maternal immune system. This results in specific immunomodulation such as fetal-antigen-dependent induction of regulatory T cells. Thus, the {"}shaping{"} of maternal immune responses by fetal antigens may represent an endogenous pathway by which antigen-specific immunomodulation might also contribute to reinstalling tolerance to autoantigens in MS. Reproductive immunology therefore has great potential to provide insights into MS immunopathogenesis and highlight novel avenues for treatment of MS and other autoimmune diseases.",
keywords = "Autoimmunity, Disease Progression, Female, Humans, Immunity, Maternally-Acquired, Immunomodulation, Multiple Sclerosis, Placental Circulation, Pregnancy, Pregnancy Complications",
author = "Konstantinos Patas and Engler, {Jan Broder} and Friese, {Manuel A} and Gold, {Stefan M}",
note = "Copyright {\textcopyright} 2012. Published by Elsevier Ireland Ltd.",
year = "2013",
month = mar,
day = "1",
doi = "10.1016/j.jri.2012.10.005",
language = "English",
volume = "97",
pages = "140--6",
journal = "J REPROD IMMUNOL",
issn = "0165-0378",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

RIS

TY - JOUR

T1 - Pregnancy and multiple sclerosis: feto-maternal immune cross talk and its implications for disease activity

AU - Patas, Konstantinos

AU - Engler, Jan Broder

AU - Friese, Manuel A

AU - Gold, Stefan M

N1 - Copyright © 2012. Published by Elsevier Ireland Ltd.

PY - 2013/3/1

Y1 - 2013/3/1

N2 - Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system of presumed autoimmune origin. Intriguingly, pregnancy in female MS patients is associated with a substantial decrease in relapse rate. However, post-partum the relapse rate increases in a rebounding fashion above the rate seen before pregnancy. Wide gaps remain in our understanding of the biological mechanisms underlying these pregnancy-related effects in MS patients. To date, most attempts to explain MS disease amelioration during pregnancy have focused on levels of circulating hormones with immunomodulatory properties such as estrogens and global shifts in systemic maternal immune cell composition. However, recent advances in our understanding of feto-maternal tolerance have provided evidence that fetal antigens directly interact with the maternal immune system. This results in specific immunomodulation such as fetal-antigen-dependent induction of regulatory T cells. Thus, the "shaping" of maternal immune responses by fetal antigens may represent an endogenous pathway by which antigen-specific immunomodulation might also contribute to reinstalling tolerance to autoantigens in MS. Reproductive immunology therefore has great potential to provide insights into MS immunopathogenesis and highlight novel avenues for treatment of MS and other autoimmune diseases.

AB - Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system of presumed autoimmune origin. Intriguingly, pregnancy in female MS patients is associated with a substantial decrease in relapse rate. However, post-partum the relapse rate increases in a rebounding fashion above the rate seen before pregnancy. Wide gaps remain in our understanding of the biological mechanisms underlying these pregnancy-related effects in MS patients. To date, most attempts to explain MS disease amelioration during pregnancy have focused on levels of circulating hormones with immunomodulatory properties such as estrogens and global shifts in systemic maternal immune cell composition. However, recent advances in our understanding of feto-maternal tolerance have provided evidence that fetal antigens directly interact with the maternal immune system. This results in specific immunomodulation such as fetal-antigen-dependent induction of regulatory T cells. Thus, the "shaping" of maternal immune responses by fetal antigens may represent an endogenous pathway by which antigen-specific immunomodulation might also contribute to reinstalling tolerance to autoantigens in MS. Reproductive immunology therefore has great potential to provide insights into MS immunopathogenesis and highlight novel avenues for treatment of MS and other autoimmune diseases.

KW - Autoimmunity

KW - Disease Progression

KW - Female

KW - Humans

KW - Immunity, Maternally-Acquired

KW - Immunomodulation

KW - Multiple Sclerosis

KW - Placental Circulation

KW - Pregnancy

KW - Pregnancy Complications

U2 - 10.1016/j.jri.2012.10.005

DO - 10.1016/j.jri.2012.10.005

M3 - SCORING: Journal article

C2 - 23432880

VL - 97

SP - 140

EP - 146

JO - J REPROD IMMUNOL

JF - J REPROD IMMUNOL

SN - 0165-0378

IS - 1

ER -