Serum Levels of Interleukin (IL)-10, IL-17, Transforming Growth Factor (TGF)-β1, and Interferon-γ Cytokines and Expression Levels of IL-10 and TGF-β1 Genes in Renal Allograft Recipients After Donor Bone Marrow Cell Infusion

2011 ◽  
Vol 43 (2) ◽  
pp. 495-499 ◽  
Author(s):  
M. Mohammadnia ◽  
G. Solgi ◽  
M. Ranjbar ◽  
T. Shahrestani ◽  
R. Edalat ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Renal Allograft ◽  
Transforming Growth Factor ◽  
Marrow Cell ◽  
Serum Levels ◽  
Interferon Γ ◽  
Donor Bone Marrow ◽  
Donor Bone Marrow Cell ◽  
Tgf Β1

Transforming Growth Factor Beta 1 Serum Levels in Patients with Preinvasive and Invasive Lesions of the Breast

2004 ◽  
Vol 19 (3) ◽  
pp. 236-239 ◽  
Author(s):  
A. Lebrecht ◽  
C. Grimm ◽  
G. Euller ◽  
E. Ludwig ◽  
E. Ulbrich ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Breast Carcinogenesis ◽  
Receptor Status ◽  
Healthy Women ◽  
Growth Factor Beta ◽  
Tgf Β1

Transforming growth factor beta (TGF-β)1 is thought to be involved in breast carcinogenesis. TGF-β1 acts in an antiproliferative manner in the early stages of breast carcinogenesis, but promotes tumor progression and metastases in the advanced stages of the disease. No data have been published on serum TGF-β1 in breast cancer. We investigated TGF-β1 serum levels in patients with breast cancer (n=135), ductal carcinoma in situ (DCIS) I to III (n=67) or fibroadenoma (n=35), and in healthy women (n=40) to determine its value as a differentiation marker between malignant, pre-invasive and benign diseases and as a predictive marker for metastatic spread. Median (range) TGF-β1 serum levels in patients with breast cancer, DCIS I-III or benign breast lesions and in healthy women were 48.8 (18–82.4) pg/mL, 45.3 (26.9–58.3) pg/mL, 47.2 (17.2–80.5) pg/mL and 51.6 (30.9–65.1) pg/mL, respectively (p=0.2). In breast cancer patients TGF-β1 serum levels showed no statistically significant correlation with tumor stage, lymph node involvement, histological grade, estrogen receptor status and progesterone receptor status. Our data fail to indicate any correlation between serum TGF-β1 levels and clinicopathological parameters of breast diseases. Serum TGF-β1 levels do not provide clinical information in addition to established tumor markers.

scholarly journals Transforming growth factor-β1 modulates responses of CD34+ cord blood cells to stromal cell-derived factor-1/CXCL12

Blood ◽  
2005 ◽  
Vol 106 (2) ◽  
pp. 485-493 ◽  
Author(s):  
Sunanda Basu ◽  
Hal E. Broxmeyer
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Cord Blood ◽  
Progenitor Cells ◽  
Stromal Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cd34 Cells ◽  
Stromal Cell Derived Factor ◽  
Tgf Β1

Abstract Disruption of stromal cell-derived factor-1 (SDF-1/CXCL12 [CXC chemokine ligand 12]) interaction leads to mobilization of stem/progenitor cells from bone marrow to circulation. However, prolonged exposure of CD34+ cells to SDF-1 desensitizes them to SDF-1. So how do cells remain responsive to SDF-1 in vivo when they are continuously exposed to SDF-1? We hypothesized that one or more mechanisms mediated by cytokines exist that could modulate SDF-1 responsiveness of CD34+ cells and the desensitization process. We considered transforming growth factor-β1 (TGF-β1) a possible candidate, since TGF-β1 has effects on CD34+ cells and is produced by stromal cells, which provide niches for maintenance and proliferation of stem/progenitor cells. TGF-β1 significantly restored SDF-1–induced chemotaxis and sustained adhesion responses in cord blood CD34+ cells preexposed to SDF-1. Effects of TGF-β1 were dependent on the dose and duration of TGF-β1 pretreatment. Phosphorylation of extracellular signal-regulated kinase 1 (Erk1)/Erk2 was implicated in TGF-β1 modulation of migratory and adhesion responses to SDF-1. Our results indicate that low levels of TGF-β1 can modulate SDF-1 responsiveness of CD34+ cells and thus may facilitate SDF-1–mediated retention and nurturing of stem/progenitor cells in bone marrow.

Down-Regulation of Toll-Like Receptor 4 Expression in Transforming Growth Factor β1 Treated Murine Dendritic Cells: Implications of Maturation Resistant to Lipopolysaccharide.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3803-3803
Author(s):  
Maofang Lin ◽  
Haibo Mou ◽  
Hong Cen
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Brdu Incorporation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Murine Bone Marrow ◽  
Gm Csf ◽  
Tgf Β1

Abstract Evidences accumulated that immature dendritic cell (iDC) could inhibit alloantigen-specific T cell responses and prolong the survival time of allografts. However, the tolerogenic properties of these iDCs were often unstable or inconsistent because of in vivo maturation, such as lipopolysaccharide (LPS) stimulating. Toll-like receptor 4(TLR4) has been reported to act as a receptor for LPS and LPS can stimulate iDC to mature DC (mDC) via TLR4 signal transduction pathway. In this study, we investigated the effects of transforming growth factor β1 on murine bone marrow derived DCs. Murine bone marrow cells were cultured with GM-CSF and TGF-β1 to generate TGF-β1 treated DCs (TGFβ-DCs). Compared to iDCs cultured by GM-CSF alone, the TGFβ-DCs had no significant alterations in ultrastructure after LPS stimulation. Surface expression of CD80, CD86, CD40, MHC-II were inhibited by addition of TGF-β1, especially in CD80, CD86 (p<0.05). Furthermore, the iDCs were sensitive to further maturation in response to LPS by showing increased levels of MHC class II, CD80, CD86 and CD40. In marked contrast, TGF-β1 prevented this LPS-mediated maturation and maintained the cells in the immature state, with low levels of surface costimulatory molecules expression. Using BrdU incorporation method, after 96 h mix lymphocyte reaction, TGFβ-DCs had weaker allogeneic stimulating capacity than iDCs. Importantly, LPS stimulating strongly promoted the allostimulatory capacity of iDCs, whereas only slightly affected TGFβ-DCs. TGFβ-DCs also showed decreased IL-12p70 production and impaired NF-κB activation after LPS stimulation. We also found the expression of TLR4 mRNA on TGFβ-DCs was weaker than that on iDCs by RT-PCR. Moreover, the results of flow cytometry revealed the positive expression percentages of TLR4/MD2 complex on iDCs and TGFβ-DCs were (51.8±3.89% vs. 15.7±4.13%, p<0.01) and the mean fluorescence intensities (MFIs) were (2.37±0.26 vs. 1.36±0.17, p<0.05). These results agreed with previous findings that TGFβ-DCs responded weakly to LPS. In summary, TGFβ-DC is resistant to maturation stimulus (LPS) and might have some correlation with the down-modulation of TLR4 expression.

Proteasome Inhibitor Bortezomib Can Inhibit Bone Marrow Fibrosis Development in a Murine Model of Myelofibrosis.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2582-2582 ◽  
Author(s):  
Orianne Wagner-Ballon ◽  
Thomas Gastinne ◽  
Micheline Tulliez ◽  
Catherine Lacout ◽  
Didier Pisani ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Proteasome Inhibitor ◽  
Transforming Growth Factor ◽  
Mice Model ◽  
Bone Marrow Fibrosis ◽  
Bortezomib Treatment ◽  
Pathway Activation ◽  
Tgf Β1 ◽  
Marrow Fibrosis

Abstract Several lines of evidence obtained from idiopathic myelofibrosis (IM) studies are in favour of a crucial role of the NF-κB pathway activation in myelofibrosis induction. It has been demonstrated that megakaryocytes, monocytes but also CD34+ cells from IM patients present a spontaneous NF-κB pathway activation associated with transforming growth factor-β1 (TGF-β1) secretion. This growth factor has been previously shown as the main fibrogenic cytokine involved in the myelofibrosis development. Mice exposed to high systemic levels of thrombopoietin (TPO) mediated by a retroviral vector (TPOhigh mice) develop a myeloproliferative disorder featuring numerous aspects of the human disease including bone marrow fibrosis, extramedullary hematopoiesis and dysmegakaryopoiesis. Moreover, TPOhigh mice display high plasma levels of IL-1α suggesting that the NF-κB pathway may play a role in this model of fibrosis. We then conducted a study to investigate whether NF-κB inhibition in this mice model could have an impact on myelofibrosis development using the proteasome inhibitor bortezomib. One month after engraftment with TPO-overexpressing hematopoietic cells, 2 groups of 20 immunocompetent C57BL/6J mice displaying similar myeloproliferation induced by TPO overexpression were constituted. Mice engrafted were treated twice a week, with either bortezomib (1 mg/kg) or a placebo for 4 weeks. At the end of this protocol, mice from both groups were examined for histological and haematological analysis including TGF-β1 and IL-1α levels determination. Here, we demonstrate that: i) the NF-κB pathway is activated in TPOhigh spleen cells and bortezomib treatment is able to inhibit this activation; ii) bortezomib treatment is able to decrease plasma concentration of TGF-β1 and IL-1α in mice as well as TGF-β1 content in extracellular fluids of marrow and spleen; iii) myelofibrosis development is inhibited after bortezomib treatment. These results emphasize the interest of developing bortezomib treatment in IM patients.

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