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T Cell Cytokines as Immunomodulators of Arthritis Disease Pathology
Published in Thomas F. Kresina, Monoclonal Antibodies, Cytokines, and Arthritis, 2020
Thomas F. Kresina, Donna J. Spannaus-Martin
In addition to the interleukins, other cytokines may mediate the inflammation of arthritis. Several hematopoietic growth factors have been reported to be present in the synovial fluid of rheumatoid arthritis patients. Granulocyte-macrophage colony stimulating factor (127), macrophage colony-stimulating factor (110), and a mast cell growth factor have been found to be present in increased amounts in the synovial fluids of patients with inflammatory arthritis. The role of these cytokines in rheumatoid arthritis is not understood at this time, but it is likely that they are involved in the modulation of the immune response. For example, granulocyte-macrophage colony stimulating factor increases Ia expression and the secretion of interleukin-1 in murine macrophages (128). The modulation of interleukin-1 secretion by this cytokine could be important in the modulation of the inflammatory response observed in arthritis.
Angiogenesis
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Insulin-like growth factor I (IGF-I) promotes chemotaxis of endothelial cells and there is evidence supporting its role in retinal neovascularization.41 A number of low molecular weight angiogenic factors (0.2 to 1 kDa) have been isolated from different sources (e.g., tumors, macrophages, serum, adipocytes).42–44 Prostaglandins are also able to stimulate angiogenesis and, furthermore, there seems to be a relation between copper ions and angiogenesis.45,46 Recently, it has been shown that macrophage colony-stimulating factor (M-CSF, 45–100 kDa) induces angiogenesis in vivo.47
The Local Immune Response in Leprosy
Published in Brian J. Nickoloff, Dermal Immune System, 2019
Jeanne Bertolli, Robert L. Modlin
γδ T cell lines established from a lesion and blood of two leprosy patients proliferated to M. leprae in vitro. To study the immunologic function of these γδ T cells, supernatants were collected from activated γδ T cell lines. These supernatants induced aggregation and cell division of bone-marrow derived macrophages treated with granulocyte macrophage-colony stimulating factor (GM-CSF). It is hypothesized that a cytokine or cytokines released from these γδ T cells synergizes with GM-CSF to induce the macrophage changes. These experiments suggest that both proliferation of γδ T cells to M. leprae antigens and secretion of cytokines which cause macrophage aggregation and proliferation are likely to be necessary for granuloma formation.
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].
The Goiânia incident, the semiotics of danger, and the next 10,000 years
Published in Clinical Toxicology, 2023
Joseph Clemons, Adam Blumenberg
Observations from serial bone marrow aspirates and biopsies corresponded with changes in granulocyte concentrations. The granulocyte recovery kinetics demonstrated a marked difference between treated and untreated individuals. Moreover, the application of granulocyte-macrophage colony-stimulating factor did not appear to influence the recovery of red blood cells or platelets. Four out of eight patients treated with granulocyte-macrophage colony-stimulating factor survived, with the fatalities being patients colonized with gram-negative bacteria prior to the initiation of granulocyte-macrophage colony-stimulating factor treatment. The side effects of granulocyte-macrophage colony-stimulating factor treatment were generally mild. Some instances of respiratory failure and/or pulmonary edema were reported during therapy, predominantly in patients with bacterial sepsis. Although these episodes were primarily attributed to infection, an effect of granulocyte-macrophage colony-stimulating factor could not be definitively excluded. Both patients who exhibited spontaneous hematological recovery survived, with one requiring forearm amputation due to severe radiation burns [15].
Colony stimulating factors for prophylaxis of chemotherapy-induced neutropenia in children
Published in Expert Review of Clinical Pharmacology, 2022
Another type of human colony stimulating factor is granulocyte-macrophage colony stimulating factor (GM-CSF). One example is sargramostim (Table 1). Similarly, GM-CSF is used to promote hematopoiesis and stimulate cellular and humoral immunity. Sargramostim stimulates hematopoietic precursor cells and increases neutrophil, eosinophil, megakaryocyte, macrophage, and dendritic cell production [24]. Compared to G-CSF, GM-CSF has similar efficacy with no difference in time to ANC recovery [27]. However, sargramostim is associated with higher frequency of clinically significant adverse effects than filgrastim such as low-grade fever, bone pain, injection site reactions, rash, headache, and diarrhea. Overall, sargramostim and filgrastim may be therapeutically equivalent and interchangeable in hospitalized patients with chemotherapy-induced neutropenia [27].