Pregnancy in multiple sclerosis: clinical and self-report scales

Neuteboom, Rinze F.; Janssens, A. Cecile J.W.; Siepman, Theodora A. M.; Hoppenbrouwers, I A; Ketelslegers, Immy A.; Jafari, Naghmeh; Steegers, Eric A.P.; Groot, Christianne de; Hintzen, Rogier Q.

doi:10.1007/s00415-011-6186-7

Cited by 27 publications

(20 citation statements)

References 22 publications

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“…However, many reports show qualitative changes in human pregnancy, including a definitive recent report studying CTL response to HCV (31). This supports clinical observations that responses to viruses such as flu and chicken pox (32,33), as well as to autoantigens, differ during pregnancy (34)(35)(36). Our conclusion is that responses are deviated during pregnancy toward more vigorous CTL responses, but this seems to have no effect on placental survival or function.…”

Section: T Cells In Pregnancysupporting

confidence: 86%

Uterine NK cells: active regulators at the maternal-fetal interface

Moffett¹,

Colucci²

2014

J. Clin. Invest.

327

301

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Pregnancy presents an immunological conundrum because two genetically different individuals coexist. The maternal lymphocytes at the uterine maternal-fetal interface that can recognize mismatched placental cells are T cells and abundant distinctive uterine NK (uNK) cells. Multiple mechanisms exist that avoid damaging T cell responses to the fetus, whereas activation of uNK cells is probably physiological. Indeed, genetic epidemiological data suggest that the variability of NK cell receptors and their MHC ligands define pregnancy success; however, exactly how uNK cells function in normal and pathological pregnancy is still unclear, and any therapies aimed at suppressing NK cells must be viewed with caution. Allorecognition of fetal placental cells by uNK cells is emerging as the key maternalfetal immune mechanism that regulates placentation. The maternal-fetal interface in the uterusThe immunological paradox of pregnancy became a central preoccupation of immunologists after the discovery of acquired immunological tolerance (1). Pregnancy and transplantation were instrumental in the discovery of MHC polymorphisms, since the best natural producers of alloantibodies against HLA molecules are multiparous women (2) and polytransfused individuals (3). Since Medawar's influential essay (4), the focus for immunologists has been how maternal T cells become tolerant of the fetal allograft. The current state of this field has been summarized in recent scholarly reviews (5, 6). We have taken a different approach that arose from studying pregnancy disorders, which affect millions of women and are a persistent global health problem. This view of the maternal immune system arose from considering how placentation evolved in mammals and is centered on the anatomy, physiology, and pathology of the pregnant uterus. We focus on the immune cells present in the pregnant uterine lining, the decidua, dominated by NK cells (known as decidual NK cells or uterine NK

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Section: T Cells In Pregnancysupporting

confidence: 86%

Uterine NK cells: active regulators at the maternal-fetal interface

Moffett¹,

Colucci²

2014

J. Clin. Invest.

327

301

View full text Add to dashboard Cite

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“…These changes are most obvious during the third trimester, when compared to the first trimester [93]. …”

Section: Reproductive Eventsmentioning

confidence: 99%

Female Gender and Reproductive Factors Affecting Risk, Relapses and Progression in Multiple Sclerosis

D’hooghe

D’Hooghe²,

Keyser

2013

Gynecol Obstet Invest

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Multiple sclerosis (MS), a chronic inflammatory demyelina-ting and degenerative disease of the central nervous system, is a frequent cause of neurological disability in young adults. Female predominance has increased over the last decades. Although female gender carries a higher risk of developing relapsing remitting MS, being female and at child-bearing age also appears to provide some protection against cognitive decline and against progressive onset MS, an adverse predictive factor when considering long-term disability in MS. The risk of MS in women has been associated with an earlier age at menarche. In most studies, parity did not impact MS risk. However, the recently published association of higher parity and offspring number with a reduced risk of a first demyelinating event suggests a potential suppressive effect. Pregnancy in MS patients has been associated with a reduced relapse rate and a reduction of neurological symptoms, especially in the third trimester. Despite the increased relapse risk in the postpartum period, there is no indication of an adverse effect of childbirth on the long-term course of MS. Fertility treatment in MS has been associated with an increased relapse risk in the following 3-month period, especially when the procedure did not result in pregnancy and gonadotrophin-releasing hormone agonists were used. Altogether, there is substantial evidence to support a regulatory role of sex steroid hormones in MS. In the absence of correlations with single hormone blood levels, we can only speculate about the underlying mechanisms. In conclusion, the increased MS risk in women and the changes in relapse and progression risk in association with reproductive events suggest significant and complex interactions between immune, neuroendocrine and reproductive systems in MS.

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“…Mean levels of total estradiol tended to be associated with disability status of women in the postmenopausal group, with lower estradiol levels being observed in the group of higher neurological impairment and vice versa; however, this association failed to reach statistical significance (23.33 ± 11.73 pg/ml vs. 14.74 ± 6.30 pg/ml, p = 0.095 in the univariate analysis and p = 0.512 after adjusting for age and years of MS). In addition, an almost significant association was observed between levels of insulin and high vs. low EDSS scores in premenopausal women (9.48 ± 6.12 μU/mL vs. 15.90 ± 10.29 μU/mL, p = 0.074 in the univariate analysis and p = 0.081 after adjusting for age and years of MS) with a statistical power of 81.9% and probability of type a error of 0.10. However, this association lost statistical significance even more after adjusting for age, BMI and glucose levels.…”

Section: Resultsmentioning

confidence: 88%