Common HLA antigens in couples with repeated abortions

Komlos, L.; Zamir, R.; Joshua, H; Halbrecht, I

doi:10.1016/0090-1229(77)90066-6

Cited by 142 publications

(40 citation statements)

References 9 publications

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“…Of these, parental incompatibility at the major histocompatibility complex (MHC) is perhaps the beststudied potential cause of early reproductive failure (review in Tregenza & Wedell 2000). Several studies have found evidence for an increased frequency of shared parental MHC antigens among human couples that have experienced high rates of early foetal loss (Komlos et al 1977;Schacter et al 1984;Ober et al 1998), and similar findings have been reported from studies of captive primates (Knapp et al 1996). There is also evidence that female mammals may be capable of sperm selection on the basis of male MHC haplotypes, suggesting avoidance of MHC incompatibility to be a potential benefit of polyandry (Wedekind et al 1996;Rü licke et al 1998;Zeh & Zeh 2001).…”

Section: Discussionmentioning

confidence: 99%

Female multiple mating behaviour, early reproductive failure and litter size variation in mammals

Stockley

2003

Proc. R. Soc. Lond. B

105

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Female promiscuity is widespread among mammals, although its function is poorly understood. Recently, much interest has been generated by the hypothesis that female promiscuity, combined with postcopulatory paternity-biasing mechanisms, may function to reduce the costs of reproductive failure resulting from genetic incompatibility. Here, a comparative approach is used to determine if average rates of reproductive failure differ for polytocous mammal species with contrasting levels of female multiple-mating behaviour. After control for phylogeny, promiscuous species were found to have significantly lower rates of early reproductive failure than monogamous and polygynous species, in which females are relatively monandrous. Monandrous females appear to compensate for higher early reproductive failure with increased ova production, and thus produce comparable average litter sizes to those of more promiscuous females. However, there is significantly more variation around the average litter sizes produced by relatively monandrous females. These findings are broadly consistent with predictions of the genetic incompatibility avoidance hypothesis, although it is emphasized that alternative explanations cannot be ruled out on the basis of the comparative evidence presented. Further studies are needed to explore ecological correlates of multiple-mating behaviour, to investigate potential post-copulatory paternity-biasing mechanisms, and to identify the causes of reproductive failure in natural mammal populations.

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Section: Discussionmentioning

confidence: 99%

Female multiple mating behaviour, early reproductive failure and litter size variation in mammals

Stockley

2003

Proc. R. Soc. Lond. B

105

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“…9 In addition, maternal-paternal immunogenetic relationships appear to influence pregnancy outcomes, 10,11 with a beneficial effect of disparity in human leukocyte antigen (HLA) genes in successful pregnancies, and a number of studies showing that excess HLA-sharing in a couple may be a risk factor for RM. [12][13][14][15] With this in mind, and extrapolating from the transplant literature in which some data suggest benefit of pre-transplant transfusion, 16 various immunotherapies have been considered for RM, aiming to modulate maternal recognition of the pregnancy. These have included paternal mononuclear cell infusion, third-party mononuclear cell infusion and administration of intravenous immune globulin.…”

Section: Introductionmentioning

confidence: 99%

Microchimerism in recurrent miscarriage

et al. 2014

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Maternal-fetal cell exchange during pregnancy results in acquisition of microchimerism, which can durably persist in both recipients. Naturally acquired microchimerism may impact maternal-fetal interaction in pregnancy. We conducted studies to ask whether microchimerism that a woman acquired from her own mother is detectable before or during pregnancy in women with recurrent miscarriage. Fetal microchimerism was also assayed. Women with primary idiopathic recurrent miscarriage (n523) and controls (n531) were studied. Genotyping was conducted for probands, their mothers and the fetus, a non-shared polymorphism identified and quantitative polymerase chain reaction performed to measure microchimerismin peripheral blood mononuclear cells. Preconception comparisons were made between recurrent miscarriage subjects and controls, using logistic regression and Wilcoxon rank sum. Longitudinal microchimerism in subsequent pregnancies of recurrent miscarriage subjects was described. There was a trend toward lower preconception detection of microchimerism in recurrent miscarriage versus controls, 6% vs. 19% (1/16 vs. 6/31, P50.2). During pregnancy, 3/11 (27%) of recurrent miscarriage subjects who went on to have a birth had detection of microchimerism from their own mother, whereas neither of two subjects who went on to miscarry had detection (0/2). This initial data suggest that microchimerism from a woman's own mother, while detectable in women with recurrent miscarriage, may differ from controls and according to subsequent pregnancy outcome. Further studies are needed to determine the cell types, quantities and any potential functional role of microchimerism in recurrent miscarriage.

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“…These observations are also quite suggestive in explaining the higher sharing of HLA antigen in couples experiencing unexplained recurrent abortion (Komlos et al 1977;Gerencer et al 1979;Beer et al 1981;Bolis et al 1984;McIntyre and Faulk 1984;Thomas et al 1985) or infertility (Jeannet et al 1985). It may be suspected that some couples experiencing recurrent abortion or infertility have combinations of the pattern which easily disturb reproductive outcomes and, as a result, higher rates of couples with shared HLA antigens may be detectable.…”

Section: Discussionmentioning

confidence: 72%