(a) Expression of intestinal metaplasia-associated genes in gastric organoids of [Stat3.sup.[DELTA]gec] or WT mice treated after stimulation with recombinant IL-6 or
IL-11 (*p < 0.05) (n = 6 organoids of WT mice, n = 3 organoids of [Stat3.sup.[DELTA]gec] mice).
IL-11, CTHRC1, miR-21, and [H.sub.2]S have been shown to help in transducing orthodontic force signals to PDLSCs.
The
IL-11 receptor gene is one of the candidate genes for osteopenia and osteoporosis.
IL-11 and granulocyte macrophage-colony stimulating factor (GM-CSF) are target genes of Runx2/CBF[beta] as OCL activators in breast cancer cells [30].
Respiratuar sinsisyal virus ile enfekte DH'ler (insan kordon kani) insuenza ile enfekte DH ile karsilastirildiginda yuksek miktarda IL-10,
IL-11 ve prostoglandin E2 ve dusuk duzeylerde proensamatuar ozellikli IL-12 salgilarlar (53).
(9,10) Cytokines such as epidermal growth factor (EGF), tumor necrosis factor alpha (TNF[alpha]), and interleukin 11 (
IL-11) have a role in the maintenance of normal cellular function and in healing and repair.
Osteolytic lesions are common in patients with either localized or multisystem involvement in Langerhans cell histiocytosis (LCH).[1] Although the skull is the more frequently affected site, virtually any bone in the body can be involved.[2] Relatively recent studies have shown that human melanoma and breast cancer cells can induce bone resorption in a murine calvaria culture system through both the direct elaboration of interleukin 11 (
IL-11) and by enhancing its production via the activation of the latent transforming growth factor [Beta] (TGF-[Beta])[3,4]; therefore, it was hypothesized that these 2 cytokines may be involved in the pathogenesis of the osteolytic lesions in LCH.
* Cytokines that may cause bone loss: IL-1, TNF, (a) IL-6,
IL-11, and ODF * Cytokines that may prevent bone loss: IL-4, IL-13, IL-18, IFN, OPG, and IL-1ra * Colony-stimulating factors: M-CSF and GM-CSF * Prostaglandins, leukotrienes, and nitric oxide * Growth factors: IGF, TGFR, FGF, PDGF, and PTHrP (a) TNF, tumor necrosis factor; CDF, osteoclast differentiation factor; IFN, interferon; M-CSF, macrophage colony-stimulating factor; GM-CSF, granulocytemacrophage colony-stimulating factor; TGF[beta], transforming growth factor-[beta]; FGF, fibroblast growth factor; PDGF, platelet-derived growth factor; PTHrP, PTH-related protein.
Many of these factors that are altered in the serum or bone marrow of MM subjects have proinflammatory activity, such as IL-1, IL-6, IL-12, IL-15, IL-16, IL-17, IL-18, IL-22, IL-23, TNF-[alpha], and IFN-[gamma], while others exert anti-inflammatory effects, such as IL-1R[alpha], IL-4, IL-10,
IL-11, TGF-[beta]1, heat-shock proteins (HSPs), and lipoxin A4.
We chose to monitor the following molecules known for their immunosuppressive capacity: IL-10,
IL-11, IDO, HGF, TGF-[beta], and LIF, and the following standard cytokines produced by MSC: IL-1[alpha], IL-1[beta], IL-6, and IL-8 produced by WJ-MSC, the last two considered biomarkers of cell senescence.
A proportion of the patients had HT before RT due to prior chemotherapy, and these patients received treatments including granulocyte-monocyte colony stimulating factor (CSF), erythropoietin (EPO) and interleukin-11 (
IL-11) before RT to ensure normal blood cell levels.