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Erschienen in: International Journal of Diabetes in Developing Countries 3/2017

08.12.2016 | Review Article

Genetic variation, biological structure, sources, and fundamental parts played by CXCL12 in pathophysiology of type 1 diabetes mellitus

verfasst von: Mojgan Noroozi Karimabad, Hossein Khoramdelazad, Gholamhossein Hassanshahi

Erschienen in: International Journal of Diabetes in Developing Countries | Ausgabe 3/2017

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Abstract

Type I diabetes (TID) is defined as an autoimmune disease resulting from the destruction of insulin-producing beta-cells by autoreactive T cells. It is believed that TID resulted from the immune-mediated destruction of insulin-producing β-cells in pancreatic islets of Langerhans. Chemokines are small glycoproteins (weighing 8–10 kDa) that are attractive chemotactive factors for a wide variety of cell types, especially immune system cells and their target cells which express appropriate G protein receptors. It has been well established that chemokines as the main arms of the immune system play key roles in the regulation of immune responses which is evidenced to be important in the pathogenesis of the diseases. Several other environmental and genetic components of the immune systems also confirmed to influence the onset of immune-related diseases. The CXC chemokine CXCL12 is involved in the development of immune responses. Previous studies reported that the known genetic variation SDF1–3′A regulates the expression of CXCL12. Hence, the aim of this study was to address the latest findings regarding the relation between the serum concentrations and CXCL12 genetic variation, in SDF1–3′A in T1D.
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Metadaten
Titel
Genetic variation, biological structure, sources, and fundamental parts played by CXCL12 in pathophysiology of type 1 diabetes mellitus
verfasst von
Mojgan Noroozi Karimabad
Hossein Khoramdelazad
Gholamhossein Hassanshahi
Publikationsdatum
08.12.2016
Verlag
Springer India
Erschienen in
International Journal of Diabetes in Developing Countries / Ausgabe 3/2017
Print ISSN: 0973-3930
Elektronische ISSN: 1998-3832
DOI
https://doi.org/10.1007/s13410-016-0534-1

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