Microchimerism and the pathogenesis of systemic sclerosis

Jl, Nelson

doi:10.1097/00002281-199811000-00010

Cited by 57 publications

(36 citation statements)

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“…Fetal microchimerism, or low levels of fetal cells persisting in the mother, is implicated in the pathogenesis of autoimmune diseases, which have a predilection for women after childbearing [18]. While basic molecular studies have implicated persisting fetal cells in the mother in some AID, supportive epidemiological evidence is limited.…”

Section: Discussionmentioning

confidence: 99%

“…The connection between fetal microchimerism and human disease was first made by Nelson, who speculated that microchimerism might be the underlying basis for the higher prevalence of autoimmune disease in women [17]. This hypothesis is supported by the similarities of chronic graft versus host disease (GVHD) to some autoimmune conditions, the prevalence of these diseases in women, their increased incidence after reproductive years, and the fact that GVHD increases with HLA incompatibility of the donor [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

“…Some authors suggest that an explanation for the conflicting results in studies relating fetal microchimerism and autoimmune disease is the migration of fetal cells preferentially into target organs of the disease rather than the circulation. Other explanations for the discrepancies in microchimerism results are differences in experimental designs and the sensitivity and specificity of the techniques used by different investigators [18]. Disease severity might also be a factor, and it may be the tissue damage of AID that leads to recruitment to and colonisation of injury sites by fetal cells, rather than autoimmunity itself [16].…”

Section: Introductionmentioning

confidence: 99%

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Pregnancy and the risk of autoimmune disease

O’Donoghue

2011

Chimerism

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Autoimmune diseases (AID) predominantly affect women of reproductive age. While basic molecular studies have implicated persisting fetal cells in the mother in some AID, supportive epidemiological evidence is limited. We investigated the effect of vaginal delivery, caesarean section (CS) and induced abortion on the risk of subsequent maternal AID. Using the Danish Civil Registration System (CRS) we identified women who were born between 1960 and1992. We performed data linkage between the CRS other Danish national registers to identify women who had a pregnancy and those who developed AID. Women were categorised into 4 groups; nulligravida (control group), women who had 1st child by vaginal delivery, whose 1st delivery was by CS and who had abortions. Log-linear Poisson regression with person-years was used for data analysis adjusting for several potential confounders. There were 1,035,639 women aged .14 years and 25,570 developed AID: 43.4% nulligravida, 44.3% had their first pregnancy delivered vaginally, 7.6% CS and 4.1% abortions. The risk of AID was significantly higher in the 1st year after vaginal delivery (RR = 1.1[1.0, 1.2]) and CS (RR = 1.3[1.1, 1.5]) but significantly lower in the 1st year following abortion (RR = 0.7[0.6, 0.9]). These results suggest an association between pregnancy and the risk of subsequent maternal AID. Increased risks of AID after CS may be explained by amplified fetal cell traffic at delivery, while decreased risks after abortion may be due to the transfer of more primitive fetal stem cells. The increased risk of AID in the first year after delivery may also be related to greater testing during pregnancy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pregnancy and the risk of autoimmune disease

O’Donoghue

2011

Chimerism

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“…FMCs were initially thought to participate in auto-immunity, since FMCs were first detected in women with systemic sclerosis and systemic lupus erythematosus, and some FMCs were T cells [Nelson, 1998;Lambert et al, 2000;Artlett et al, 2002]. However, this was not substantiated in better controlled studies [Evans et al, 1999;Ichikawa et al, 2001;Gannage et al, 2002], while FMCs were also found in a range of non-auto-immune diseases [Johnson et al, 2002;Cha et al, 2003;.…”

Section: Introductionmentioning

confidence: 99%

Microchimeric Fetal Cells Are Recruited to Maternal Kidney following Injury and Activate Collagen Type I Transcription

Bou‐Gharios

Amin²,

Hill³

et al. 2010

Cells Tissues Organs

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Fetal cells enter the maternal circulation from the early first trimester of pregnancy, where they persist in tissue decades later. We investigated in mice whether fetal microchimeric cells (FMCs) can be detected in maternal kidney, and whether they play a role in kidney homeostasis. FMCs were identified in vivo in two models: one an adaptive model following unilateral nephrectomy, the other an injury via unilateral renal ischaemia reperfusion. Both models were carried out in mothers that had been mated with transgenic mice expressing luciferase transgene under the control of collagen type I, and had given birth to either 1 or 3 litters. FMCs were detected by Y-probe fluorescent in situ hybridization (FISH) and bioluminescence, and the cell number quantified by real-time polymerase chain reaction. In the adaptive model, the remaining kidney showed more cells by all 3 parameters compared with the nephrectomized kidney, while ischaemia reperfusion resulted in higher levels of FMC participation in injured compared to contralateral kidneys. Bioluminescence showed that FMCs switch on collagen type I transcription implicating mesenchymal lineage cells. After injury, Y-probe in situ hydridization was found mainly in the tubular epithelial network. Finally, we compared FMCs with bone marrow cells and found similar dynamics but altered distribution within the kidney. We conclude that FMCs (1) are long-term sequelae of pregnancy and (2) are recruited to the kidney as a result of injury or adaptation, where they activate the transcriptional machinery of matrix proteins.

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“…Já foi demonstrado que os hormônios sexuais apresentam efeitos na função imunológica e na autoimunidade (5) ; entretanto, apenas as diferenças nos hormônios sexuais entre homens e mulheres parecem não ser suficientes para explicar a predominância feminina em doenças autoimunes. Gravidez é um evento unicamente feminino com drásticas mudanças hormonais; a exposição a células fetais representa um evento imunológico, uma vez que essas células expressam produtos genéticos que são herdados do pai, sendo, então, estranhos para a mulher grávida (6) . A doença enxerto-versus-hospedeiro (GVHD) crônica, após transplante de células tronco, é uma condição de quimerismo e apresenta similaridades com algumas doenças auto-imunes.…”

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Microquimerismo fetal-materno nas doenças reumáticas auto-imunes

Barcellos¹,

Andrade²

2004

Rev. Bras. Reumatol.

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REVIEW ARTICLE RESUMOEstudos recentes indicam a existência de um tráfego bidirecional de células durante a gestação humana normal. Células fetais persistem no sangue periférico materno por muitos anos após a gestação. Muitas doenças auto-imunes são mais prevalentes em mulheres, algumas das quais apresentam pico de incidência em fases tardias dos anos férteis femininos. A doença enxerto-versushospedeiro é uma condição conhecida de quimerismo e possui similaridades clínicas com algumas doenças auto-imunes reumáticas, notavelmente com esclerose sistêmica e síndrome de Sjögren e, algumas vezes, com lúpus eritematoso sistêmico. Este artigo explora a hipótese de que o microquimerismo fetal contribua para a patogênese de algumas doenças auto-imunes, baseado em revisões de estudos anteriores que trabalharam com esta hipótese. São apresentadas ressalvas de ordem conceitual e técnica a serem consideradas na interpretação dos dados da literatura.Palavras-chave: microquimerismo, doença reumática autoimune, auto-imunidade, esclerose sistêmica, lúpus eritematoso sistêmico.

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Microchimerism and the pathogenesis of systemic sclerosis

Cited by 57 publications

References 0 publications

Pregnancy and the risk of autoimmune disease

Pregnancy and the risk of autoimmune disease

Microchimeric Fetal Cells Are Recruited to Maternal Kidney following Injury and Activate Collagen Type I Transcription

Microquimerismo fetal-materno nas doenças reumáticas auto-imunes

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