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Synovial Fluid
Published in Verna Wright, Eric L. Radin, Mechanics of Human Joints, 2020
Pierre Geborek, Frank A. Wollheim
Cytokines have been identified in SF. However, their cellular origins often remain speculative. Also, their physiological role in the inflammed joint remains uncertain because of their multiple functions and target cells. A tentative functional classification was suggested by Harris. Interleukin-2, interleukin-3, interleukin-4, and interferon-γ are produced by Tlymphocytes, and their functions relate to activation and amplification of cellular and humoral immune responses. Interleukin-1, interleukin-6, colony-stimulating factor 1, and tumor necrosis factor a originate from macrophages-fibroblasts, and they have broad effects on cells, resulting in proliferation, increased prostaglandin formation, protease activity, bone resorption, and fever. Interestingly, cytokines originating from lymphocytes seem to be low in SF, whereas those from macrophages-fibroblasts are high. The hypothesis has been that macrophage-fibroblast originating substances inhibit lymphocyte cytokines, at least in rheumatoid joints (52).
The Role of Filgrastim
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Fabio Scarpellini, Marco Sbracia
G-CSF belongs to the group of colony stimulating factors (CSFs), macrophage colony-stimulating factor (M-CSF or CSF1), granulocyte-macrophage stimulating factor (GM-CSF or CSF2), and granulocyte colony-stimulating factor (G-CSF or CSF3). The CFSs are a group of glycoproteins that bind to specific receptors on HSCs, promoting cell proliferation and differentiation into macrophages and granulocytes. They show different structures, gene location, and different receptors. All CSFs are involved in the reproductive process from ovulation to implantation and pregnancy [2]. G-CSF is a glycoprotein of 174–180 amino acids long and with a molecular weight of 19,600 Dalton: its gene is located on the long arm of chromosome 17, in region 17q11.2-q12.8 [15]. It binds to a specific receptor, the G-CSF R or CD114, encoded by a gene on the short arm of chromosome 1 in the region 1p35–34.3. G-CSF is a protein 836 amino acids long and of 92,156 Daltons molecular weight [16]. The GCSF-R is associated with signal transduction through the JAK-STAT3 pathways. G-CSF and its receptor have been found on trophoblasts and in the decidua of several mammals, including human placenta [17,18]. An anti-abortive role has been demonstrated for G-CSF in animal models, and its depletion is indirectly involved in miscarriages [19,20]. It has also been shown that G-CSF has a positive effect on trophoblast metabolism [21]. Furthermore, G-CSF is secreted in follicular fluid and its levels correlated with oocyte competence and the implantation potential of corresponding embryos [22].
Immune Control of Myometrial Contractility: Role of Mast Cells
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
Certain cytokines can function as chemoattractants for macrophages. Colony stimulating factor-1, transforming growth factor-β, and tumor necrosis factor-a have all been shown to enhance migration of monocytes to the uterus.64–66 Because the macrophage also produces these cytokines, an autocrine feedback loop appears likely. Estrogen also can stimulate migration of macrophages into the uterus, either directly or by indirect stimulation of cytokines.67
Dysregulated metabolism: A friend-to-foe skewer of macrophages
Published in International Reviews of Immunology, 2023
Keywan Mortezaee, Jamal Majidpoor
Colony stimulating factor-1 (GSF-1) (also called macrophage-colony stimulating factor (M-CSF) interacts with CSF-1R for regulation of macrophage differentiation, survival and migration. CSF-1R is belonged to the receptor protein tyrosine kinase that is contributed to the induction of many types of proto-oncogenes [8]. Autocrine consumption of CSF-1 by differentiating MΦ cells is augmented under lactate exposure. In fact, under lactate exposure, expression of CD163 in macrophages is reinforced by CSF-1 and IL-6, indicating their contribution to the acquisition of M2-like phenotype in macrophages [69]. CSF-1 is highly presented in PDAC. CSF-1 inhibitors reduce the number of CD206 high TAMs in murine PDAC. Presence of CD206 high TAMs in human counterpart is associated with the poor clinical outcomes [104]. CSF-1R blockade in mouse model of breast cancer stimulates an inflamed type I IFN response and augments the efficacy of platinum-based chemotherapy [105]. CSF-1 is also released from GBM cells and turns macrophages into ‘bad macrophages’, while administration of the CSF-1R inhibitor BLZ945 mitigates tumor-promoting TAMs [106] and suppresses tumor progression [107].
MEOX2 serves as a novel biomarker associated with macrophage infiltration in oesophageal squamous cell carcinoma and other digestive system carcinomas
Published in Autoimmunity, 2021
Zhen Wang, Han Yang, Rusi Zhang, Bin Luo, Bingchen Xu, Zhihua Zhu, Peng Lin
Colony-stimulating factor 1 (CSF-1) is essential for the proliferation and differentiation of macrophages. Thus, we explored correlations between the mRNA expression of MEOX2 and the mRNA expression of colony-stimulating factor 1 (CSF-1) and colony-stimulating factor 1 receptor (CSF-1R) with the TIMER database. The results showed that MEOX2 expression exhibited positive correlations with the mRNA expression of CSF-1 (r = 0.336, p = 2.84e-6) and CSF-1R (r = 0.475, p = 8.07e-12) in oesophageal carcinoma. Further analysis indicated that in the other digestive system carcinomas, MEOX2 expression exhibited positive correlations with the mRNA expression of CSF-1 and CSF-1R, and the correlations in these kinds of carcinomas were even more obvious (Table 2, Figure 7).
Therapeutic targets for liver regeneration after acute severe injury: a preclinical overview
Published in Expert Opinion on Therapeutic Targets, 2020
Hidenobu Kojima, Kojiro Nakamura, Jerzy W. Kupiec-Weglinski
Colony-stimulating factor 1 (CSF1) was measured in serum samples from 55 patients after hepatic resection and 78 patients with acetaminophen overdose acute liver failure [84]. Serum CSF1 levels increased in patients with hepatic resection in proportion to the resected liver volume, and a low serum CSF1 level was associated with worse prognosis (King’s College criteria) and increased mortality/transplantation in patients with acetaminophen overdose acute liver failure. Serum CSF1 level was a better predictor than HMGB1 released by necrotic cells and proposed as a prognostic marker for ALF [85]. Furthermore, as subcutaneous CSF1-Fc administration promoted the macrophage accumulation and liver regeneration in mice with acetaminophen acute liver injury [84], CSF1 could be not only a prognostic marker, but also a therapeutic target for liver regeneration in ALF. Indeed, recombinant human macrophage-CSF was apparently well tolerated in humans [86].