Alpha cells, the main source of IL-1β in human pancreas.
Alpha cells, the main source of IL-1β in human pancreas.
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DOI：
10.1016/j.jaut.2017.03.006
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发表时间：
2017-07
影响因子：
12.8
通讯作者：
von Herrath MG
中科院分区：
文献类型：
--
作者：
Anquetil F;Sabouri S;Thivolet C;Rodriguez-Calvo T;Zapardiel-Gonzalo J;Amirian N;Schneider D;Castillo E;Lajevardi Y;von Herrath MG
白细胞介素-1 β（IL-1β）在体外可引起β细胞功能障碍，并可能在1型糖尿病和2型糖尿病的发病过程中发挥作用。然而，几项试图阻断IL-1β功能的临床试验取得的成功微乎其微。因此，我们重新研究了IL-1β在人类糖尿病和非糖尿病胰腺中的局部表达。我们从患有糖尿病的胰腺器官供体网络（nPOD）获得胰腺组织切片，包括非糖尿病对照（n=9）、非糖尿病自身抗体阳性（AAb+，n=5）、1型糖尿病（n=6）和2型糖尿病（n=6）供体。用原位杂交法和间接免疫荧光法分别检测IL-1β mRNA和IL-1β蛋白的表达。我们发现，在非糖尿病和糖尿病供体中，胰岛内IL-1β的产生水平相当。有趣的是，IL-1β的主要来源是α细胞，而不是β细胞。我们的研究结果对IL-1β在糖尿病胰腺中的作用提出了质疑，因为它已经在以前的文献中提出。此外，我们关于IL-1β定位的结果应导致进一步研究IL-1β在胰腺α细胞生理学中的作用。
Interleukin-1β (IL-1β) is known to trigger beta cell dysfunction in vitro and could potentially play a role during the pathogenesis of type 1 diabetes and type 2 diabetes. However, several clinical trials attempting to block IL-1β function have had minimal success. We therefore reinvestigated local expression of IL-1β in human diabetic and non-diabetic pancreata. We obtained pancreatic tissue sections from the Network for Pancreatic Organ Donors with Diabetes (nPOD) including non-diabetic control (n=9), non-diabetic auto-antibody positive (AAb+, n=5), type 1 diabetes (n=6), and type 2 diabetes (n=6) donors. Islets were systematically investigated for the presence of IL-1β mRNA by in situ hybridization and IL-1β protein by indirect immunofluorescence. We found that intra-islet IL-1β was produced at comparable levels in both non-diabetic and diabetic donors. Interestingly, the main source for IL-1β was alpha cells but not beta cells. Our findings call into question the role of IL-1β in the diabetic pancreas as it has been proposed in previous literature. Additionally, our results regarding the localization of IL-1β should lead to further investigation into the role of IL-1β in the physiology of pancreatic alpha cells.
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影响因子：
3.7
作者：
Marselli L;Thorne J;Dahiya S;Sgroi DC;Sharma A;Bonner-Weir S;Marchetti P;Weir GC
通讯作者：
Weir GC
影响因子：
7.7
作者：
Welsh, N;Cnop, M;Eizirik, DL
通讯作者：
Eizirik, DL
影响因子：
168.9
作者：
Moran, Antoinette;Bundy, Brian;Becker, Dorothy J.;DiMeglio, Linda A.;Gitelman, Stephen E.;Goland, Robin;Greenbaum, Carla J.;Herold, Kevan C.;Marks, Jennifer B.;Raskin, Philip;Sanda, Srinath;Schatz, Desmond;Wherrett, Diane K.;Wilson, Darrell M.;Krischer, Jeffrey P.;Skyler, Jay S.;Pickersgill, Linda;de Koning, Eelco;Ziegler, Anette-G;Boeehm, Bernhard;Badenhoop, Klaus;Schloot, Nanette;Bak, Jens Friis;Pozzilli, Paolo;Mauricio, Didac;Donath, Marc Y.;Castano, Luis;Waegner, Ana;Lervang, Hans Henrik;Perrild, Hans;Mandrup-Poulsen, Thomas
通讯作者：
Mandrup-Poulsen, Thomas
影响因子：
4.8
作者：
Boeni-Schnetzler, Marianne;Boller, Simone;Donath, Marc Y.
通讯作者：
Donath, Marc Y.
DOI：
10.1016/j.clim.2013.02.003
发表时间：
2013-12
期刊：
Clinical immunology (Orlando, Fla.)
影响因子：
--
作者：
Nepom GT;Ehlers M;Mandrup-Poulsen T
通讯作者：
Mandrup-Poulsen T