scholarly journals Alternate Splicing of Interleukin-1 Receptor Type II (IL1R2) In Vitro Correlates with Clinical Glucocorticoid Responsiveness in Patients with AIED

PLoS ONE ◽  
2009 ◽  
Vol 4 (4) ◽  
pp. e5293 ◽  
Author(s):  
Andrea Vambutas ◽  
James DeVoti ◽  
Elliot Goldofsky ◽  
Michael Gordon ◽  
Martin Lesser ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Receptor Type ◽  
Type Ii ◽  
Alternate Splicing

scholarly journals Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology

Reproduction ◽  
2007 ◽  
Vol 134 (3) ◽  
pp. 525-534 ◽  
Author(s):  
S Guay ◽  
A Akoum
Keyword(s):  
Interleukin 1 ◽  
Receptor Type ◽  
Type Ii ◽  
Endometrial Cells ◽  
Functional Changes ◽  
Empty Vector ◽  
Ishikawa Cells ◽  
Empty Expression Vector

Our previous studies showed a marked deficiency in interleukin 1 receptor type II (IL1R2) in the endometrial tissue of women with endometriosis, particularly in epithelial cells. We believe that such a deficiency in IL1R2, a potent and specific IL1 inhibitor, makes endometrial cells more sensitive to IL1 and less capable of buffering the cytokine’s effects, which may lead to functional changes that favor endometriosis development. The main objective of our study was to stably inhibit IL1R2 expression in endometrial cells in order to evaluate the role of IL1R2 deficiency in endometriosis pathophysiology. Stable clones of Ishikawa adenocarcinoma endometrial cells transfected with IL1R2 antisense and showing downregulation of IL1R2 protein expression, or with the empty expression vector alone and showing no noticeable difference in IL1R2 expression, were selected. The downregulation of IL1R2 expression in IL1R2 antisense transfectants when compared with control cells was confirmed by ELISA, Western blot and immunofluorescence. In these cells, IL1R2 expression was markedly reduced, compared with non-transfected cells or cells transfected with the empty vector, and there was a significant increase in the basal and the IL1-β (IL1B)-induced levels of matrix metalloproteinase (MMP)-2 and MMP-9 secretion. Furthermore, a significant decrease in IL1B-induced secretion of tissue inhibitor of MMPs-1, a known MMP-9 inhibitor, was observed. These in vitro data make plausible a role for IL1R2 deficiency in the capability of endometrial cells to invade the host tissue and develop in ectopic locations.

White matter lesions and soluble interleukin-1 receptor type II in CSF from demented and non-demented subjects

2002 ◽  
Vol 41 (4) ◽  
pp. 217-222 ◽  
Author(s):  
Lena Bronge ◽  
Lars-Olof Wahlund ◽  
Annelie Brauner ◽  
Hans Basun ◽  
Anita Garlind
Keyword(s):  
White Matter ◽  
Interleukin 1 ◽  
White Matter Lesions ◽  
Receptor Type ◽  
Type Ii

Soluble interleukin-1 receptor type II levels are elevated in cerebrospinal fluid in Alzheimer's disease patients

1999 ◽  
Vol 826 (1) ◽  
pp. 112-116 ◽  
Author(s):  
Anita Garlind ◽  
Annelie Brauner ◽  
Bo Höjeberg ◽  
Hans Basun ◽  
Marianne Schultzberg
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Interleukin 1 ◽  
Receptor Type ◽  
Type Ii

scholarly journals Hematopoietic growth factors upregulate the p65 type II interleukin-1 receptor on bone marrow progenitor cells in vitro

Blood ◽  
1992 ◽  
Vol 80 (3) ◽  
pp. 600-608 ◽  
Author(s):  
CM Dubois ◽  
FW Ruscetti ◽  
SE Jacobsen ◽  
JJ Oppenheim ◽  
JR Keller
Keyword(s):  
Bone Marrow ◽  
Growth Factors ◽  
Progenitor Cells ◽  
Specific Binding ◽  
Interleukin 1 ◽  
Scatchard Analysis ◽  
Type I ◽  
Type Ii ◽  
Hematopoietic Growth Factors

Abstract Having previously shown that interleukin-1 (IL-1) induces the expression of IL-1 receptors (IL-1Rs) on bone marrow (BM) cells in vivo through an indirect mechanism, we studied whether hematopoietic growth factors (HGFs) could induce the expression of IL-1R on BM cells in vitro. In vitro treatment of light-density murine BM (LDBM) cells with either IL-3, IL-6, granulocyte--colony-stimulating factor (CSF), or granulocyte-macrophage--CSF caused a 5- to 10-fold upregulation of IL- 1R expression, whereas IL-1, IL-5, IL-7, and macrophage-CSF had no effect. Scatchard analysis showed one class of IL-1Rs on LDBM cells with an average of 66 +/- 20 sites per cells. After 24 hours of treatment with IL-3, the number of IL-1Rs increased to 413 +/- 125, without effecting the affinity. This effect required protein synthesis, but was independent of cell division. Purified lineage-negative progenitor cells (Lin-) did not express detectable levels of IL-1R, but 24 hours of treatment with IL-3, GM-CSF, and G-CSF stimulated IL-1-- specific binding. Autoradiographic analysis of Lin- cells showed that IL-1R induction by IL-3 occurs on undifferentiated blast cells. Affinity labeling of Lin- cells treated with HGFs showed an increase in a 65-Kd IL-1 binding protein that did not bind or compete with an anti- type I IL-1R antibody, suggesting that these cells expressed type II IL- 1R. These data suggest that IL-1 stimulation of myelopoiesis occurs by a mechanism involving IL-1R upregulation on hematopoietic progenitor cells by HGFs.

Imbalance in the peritoneal levels of interleukin 1 and its decoy inhibitory receptor type II in endometriosis women with infertility and pelvic pain

2008 ◽  
Vol 89 (6) ◽  
pp. 1618-1624 ◽  
Author(s):  
Ali Akoum ◽  
Mahéra Al-Akoum ◽  
André Lemay ◽  
Rodolphe Maheux ◽  
Mathieu Leboeuf
Keyword(s):  
Pelvic Pain ◽  
Interleukin 1 ◽  
Receptor Type ◽  
Type Ii ◽  
Inhibitory Receptor

Expression of Transforming Growth Factor β1, β2, and β3 in Chronic, Cancer-Associated, Obstructive Pancreatitis

2006 ◽  
Vol 130 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Yuki Fukumura ◽  
Toshio Kumasaka ◽  
Keiko Mitani ◽  
Kanae Karita ◽  
Koichi Suda
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Early Stage ◽  
Smooth Muscle Actin ◽  
Receptor Type ◽  
Type Ii ◽  
Soluble Receptor ◽  
Obstructive Pancreatitis ◽  
Tgf Β1

Abstract Context.—Myofibroblasts are considered to play central roles in pancreatic fibrosis. The potent fibrogenic capacities of transforming growth factor βs (TGF-βs) have been emphasized in vitro and in animal studies. However, the roles of TGF-βs in human chronic pancreatitis have not been fully clarified. Objective.—To investigate whether expressions of TGF-βs are related to myofibroblast distribution in chronic, cancer-associated, obstructive pancreatitis (COP). Design.—Histopathologic studies using hematoxylin-eosin and Elastica-Masson trichrome and immunohistochemical studies using antibodies against α-smooth muscle actin (SMA); CD68; TGF-β1, -β2, and -β3; and TGF-β soluble receptor type II were performed in 19 COP cases and 6 controls. By classifying COP tissues into 3 fibrosis phases by the amount of collagen deposits, immunoreactivities for TGF-βs, histopathologic changes, and myofibroblast distribution were examined for each fibrosis phase. Results.—Six cases were categorized in the early stage of fibrosis, 8 in the intermediate stage, and 5 in the advanced stage. Immunoreactivities for all 3 isoforms of TGF-β were observed in occasional myofibroblasts. In the early and intermediate stages, TGF-β1–expressing macrophages and neutrophils were distributed in the midst of myofibroblasts. TGF-β2 and TGF-β3 expressions were observed in ductal structures, sometimes even in sites where no or few myofibroblasts were seen. TGF-β soluble receptor type II was immunoreactive for myofibroblasts, endothelium, and ductal structures. Conclusions.—All 3 isoforms of TGF-βs may contribute to fibrosis in COP. Macrophages and neutrophils may be sources of fibrogenic TGF-β1. Infiltration of these cells appears to play an important role in the progression of COP fibrosis.

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