Detection of maternal-fetal microchimerism in the inflammatory lesions of patients with Sjogren's syndrome

Kuroki, M; Okayama, Akira; Nakamura, Seiji; Sasaki, Takashi; Murai, Koichi; Shiba, Ryosuke; Shinohara, Masanori; Tsubouchi, Hirohito

doi:10.1136/ard.61.12.1041

Cited by 48 publications

(37 citation statements)

References 22 publications

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“…Although FMc is not limited to autoimmune disease, some studies have found a significant increase of FMc in Sjogren's syndrome (in labial salivary glands), systemic lupus (in kidney), and Hashimoto's disease (in thyroid; refs. 6,8,9). In functional studies of fetal T-cell clones derived from maternal blood, FMc reactive to maternal HLA was observed more frequently in women with systemic sclerosis than normal women (10).…”

Section: Introductionmentioning

confidence: 99%

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Fetal Microchimerism in Women with Breast Cancer

2007

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Fetal microchimerism (FMc) describes long-term persistence of small numbers of fetal-derived allogeneic cells in the mother. Although FMc has been implicated as a mechanism of autoimmune disease, it may confer a beneficial effect with immune surveillance of malignant cells. We hypothesized that allogeneic FMc imparts a protective effect against breast cancer. Two observations provided a rationale for the study hypothesis. First, allogeneic cells convey risk reduction for recurrent malignancy in hematopoietic cell transplantation. Second, reduced risk of breast cancer is well recognized among parous compared with nulliparous women. As an initial test of the hypothesis, we investigated 82 women, 35 with breast cancer and 47 who were healthy, for male DNA in peripheral blood, presumed from a prior pregnancy with a male fetus. The prevalence and levels of male DNA were determined by real-time quantitative PCR for the Y chromosome-specific gene DYS14 in DNA extracted from peripheral blood mononuclear cells. FMc was found significantly more often in healthy women than women with breast cancer (43% versus 14%, respectively). Considering the absence of FMc as a risk factor, the odds ratio was 4.4 [95% confidence intervals (95% CI), 1.34-16.99; P = 0.006]. Restricting analysis to women known to had given birth to a son, the odds ratio was 5.9 (95% CI, 1.26-6.69; P = 0.01). Our findings indicate that allogeneic FMc may contribute to reduction in risk of breast cancer. Further studies are indicated and, if confirmed, extended studies to examine whether allogeneic immune surveillance from FMc is deficient in women with breast cancer. [Cancer Res 2007;67(19):9035-8]

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Section: Introductionmentioning

confidence: 99%

“…[2][3][4][5][6]. FMc is usually semiallogeneic to the mother and because autoimmune diseases are more prevalent in women, FMc has been investigated recently in several autoimmune diseases.…”

Section: Introductionmentioning

confidence: 99%

Fetal Microchimerism in Women with Breast Cancer

2007

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“…It was recently reported that the Y-chromosome DNA of fetus origin (maternal-fetal microchimerism) was found in the peripheral blood of female patients with lupus nephritis (Mosca et al 2003) and in the salivary glands and lungs of female patients with Sjögren's syndrome (Kuroki et al 2002). Our observations suggest that fetal cells not only enter the maternal circulation, but also comprise a proportion of differentiated renal cells, such as those of the extraglomerular mesangium and renal tubular epithelium.…”

Section: Discussionmentioning

confidence: 56%

“…Since the fetal chimeric cells could be involved in maternal allogeneic tolerance to the fetus, the fetal chimeric cells might be implicated in maternal-fetal immunology and development of maternal autoimmune diseases. This fetal microchimerism has been proposed to contribute to the etiology of autoimmune diseases such as systemic sclerosis (Burastero et al 2003), Sjögren's syndrome (Kuroki et al 2002), and primary biliary cirrhosis (Fanning et al 2000). However, the mechanism by which role of fetal microchimerism participates in disease onset is unknown.…”

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confidence: 99%

Detection of Fetal Cells in the Maternal Kidney during Gestation in the Mouse

Matsubara

Uchida

Matsubara

et al. 2009

Tohoku J. Exp. Med.

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“…One possible explanation is the microchimerism, which consists on the presence of circulating donor and recipient hematopoietic cells. Studies showed that the male donor cells may initiate GVHD [15,17]. In agreement with the European Group for Blood and Marrow Transplantation, male recipients with female donors presented the worst outcome after HSCT, relative to all other donor-recipient gender combinations [12].…”

Section: Discussionmentioning

confidence: 76%

Cytokine Production and Human Cytomegalovirus Load in Allogeneic Hematopoietic Stem Cell Transplantation Outcome

TA¹

2016

Int J Immunother Cancer Res

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Objective: To investigate the impact of cytokine levels (IL-1β, IL-6, IL-10, IFN-γ and TNF-α) and Human cytomegalovirus (HCMV) load in the saliva and blood on the survival of allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipients.Study Design: Samples were obtained from 63 patients 7 days before and 21 days after allo-HSCT. Cytokine levels were assessed by ELISA, and HCMV load was determined by real-time PCR. Results:The increase of IL-6 in the saliva and the reduction of IFN-γ in the blood before allo-HSCT were associated with increased risk of death. Moreover, the increase of IL-6 in the blood and of HCMV in the saliva after allo-HSCT were also associated with increased risk of death. Conclusions:Cytokine levels and HCMV load were associated with the increased risk of death. The findings suggest a potential function of these biomarkers in the determination of allo-HSCT survival.factor-α (TNF-α) and interleukin-1 (IL-1), could be increased as a result of disease, therapy, comorbidities or ongoing infections that occur before allo-HSCT. Second, immediately after allo-HSCT, the immune dysfunction caused by the conditioning regimen, which may produce tissue injury and consequently the production of inflammatory cytokines, may affect the reconstitution of white blood cells. Third, after allo-HSCT, activated, mature donor T-cells can set off a cytokine response that in turn stimulates host T-cell responses related to the onset of acute graft-versus-host disease (aGVHD) [3,4]. Immune dysfunction following allo-HSCT involves activated T-cells secreting interferon (IFN)-γ as well as other cytokines, which activate monocytes and dendritic cells. This process appears to be associated with the induction of aGVHD, resulting in significant morbidity and mortality. In addition, a prolonged immune deficiency characterized by lymphopenia and susceptibility to infection can occur [2]. Deregulation of inflammatory cytokines is also associated with multiple symptoms (pain, sleep disturbance and depression) during neutropenia after allo-HSCT [3]. Interleukin-6 (IL-6) is an important pro-inflammatory cytokine involved in immune-mediated complications after allo-HSCT [5].Human cytomegalovirus (HCMV) infection remains one of the most important causes of morbidity and mortality among allo-HSCT recipients [6,7]. Infection by HCMV may result not only in HCMV disease, but is also associated with other adverse effects due to its immunomodulatory actions; this might result in increased risk of bacterial, fungal and viral infections, and also of aGVHD [8].Allo-HSCT outcomes could be affected by factors such as HCMV infection, recipient/donor histocompatibility, patient/donor gender,

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Detection of maternal-fetal microchimerism in the inflammatory lesions of patients with Sjogren's syndrome

Cited by 48 publications

References 22 publications

Fetal Microchimerism in Women with Breast Cancer

Fetal Microchimerism in Women with Breast Cancer

Detection of Fetal Cells in the Maternal Kidney during Gestation in the Mouse

Cytokine Production and Human Cytomegalovirus Load in Allogeneic Hematopoietic Stem Cell Transplantation Outcome

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