Why are levels of maternal microchimerism higher in type 1 diabetes pancreas?

Vanzyl, Berendine; Planas, Raquel; Ye, Jody; Foulis, Alan K.; Krijger, Ronald R. de; Vives-Pi, Marta; Gillespie, Kathleen M.

doi:10.4161/chim.1.2.13891

Cited by 24 publications

(33 citation statements)

References 20 publications

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“…Studies of patients with recent-onset type 1 diabetes have identified a higher number of maternal cells in the periphery and in the pancreas compared with controls [107,108]. Maternal cells in the islets of deceased patients with recent-onset type 1 diabetes did not have an immune origin, which argues against activation of maternal immune cells [108].…”

Section: Some Mechanisms Of Potential Relevancementioning

confidence: 99%

“…Maternal cells in the islets of deceased patients with recent-onset type 1 diabetes did not have an immune origin, which argues against activation of maternal immune cells [108]. One hypothesis is that the increased numbers of maternally derived cells are due to an attempt to replace beta cells lost to as a result of immune attack [107].…”

Section: Some Mechanisms Of Potential Relevancementioning

confidence: 99%

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The prenatal environment and type 1 diabetes

Stene

Gale

2013

Diabetologia

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Section: Some Mechanisms Of Potential Relevancementioning

confidence: 99%

Section: Some Mechanisms Of Potential Relevancementioning

confidence: 99%

The prenatal environment and type 1 diabetes

Stene

Gale

2013

Diabetologia

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“…In pancreas samples obtained from 6 males with T1DM Vanzyl et al [296] found that the frequency of MMc was significantly higher (range 0.32-0.80%, mean 0.58%) than in 4 male controls (0.24-0.50%, mean 0.38%; p=0.05). Interestingly, clusters of 2-3 MMc were occasionally found in the pancreases, particularly T1DM pancreases, suggesting replication of these cells [296].…”

Section: Diabeticsmentioning

confidence: 95%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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“…63 In the pancreas from diabetic children, maternal Mc cells were insulin producing islet cells and not hematopoietic CD45 + . 64 This absence of hematopoietic cells is against the idea that maternal cells directly react against fetal/offspring tissues in the context of autoimmunity. However, they might influence the offspring's immune system in other ways.…”

Section: Possible Roles Of Maternal Microchimeric Cells On the Contrimentioning

confidence: 99%