“…CD54 (ICAM-1) is a macrophage activation marker [15] that functions as a ligand for leukocyte integrin complex to facilitate cell-cell interactions. CD54 expression is reported to be up regulated upon stimulation with macrophage stimulating factors such as GM-CSF, TLR3, TLR4 and TLR7 [14]. RBL upregulated CD54 expression in THP-1 cells comparable with the level induced by the combined treatment of PMA and LPS.…”
Section: Discussionmentioning
confidence: 69%
“…One of the initial events in the differentiation of monocytes to macrophage is increased adherence [14]. The kinetics of adhesion of THP-1 monocytes revealed that RBL-induced cell adhesion was delayed compared to cells stimulated with PMA.…”
Section: Discussionmentioning
confidence: 97%
“…Increased adherence is a functional indicator of macrophage differentiation [14]. The effect of RBL on adhesion was studied at two time points -6 h and 12 h. As shown in Fig.…”
“…CD54 (ICAM-1) is a macrophage activation marker [15] that functions as a ligand for leukocyte integrin complex to facilitate cell-cell interactions. CD54 expression is reported to be up regulated upon stimulation with macrophage stimulating factors such as GM-CSF, TLR3, TLR4 and TLR7 [14]. RBL upregulated CD54 expression in THP-1 cells comparable with the level induced by the combined treatment of PMA and LPS.…”
Section: Discussionmentioning
confidence: 69%
“…One of the initial events in the differentiation of monocytes to macrophage is increased adherence [14]. The kinetics of adhesion of THP-1 monocytes revealed that RBL-induced cell adhesion was delayed compared to cells stimulated with PMA.…”
Section: Discussionmentioning
confidence: 97%
“…Increased adherence is a functional indicator of macrophage differentiation [14]. The effect of RBL on adhesion was studied at two time points -6 h and 12 h. As shown in Fig.…”
“…However, it is known that CD93 (C1qRp) is a transmembrane receptor regulating phagocytosis and cell adhesion and is present on cells of the myeloid lineage (45). CD93 expression is increased with monocyte differentiation and macrophage activation (46,47). Targeting of Cd93 mRNA by miR-29 could promote commitment to osteoclastogenesis, preventing monocytic differentiation.…”
Section: Discussionmentioning
confidence: 99%
“…8E). NFIA expression inhibits both macrophage and osteoclast maturation, whereas GPR85 and CD93 are expressed during macrophage differentiation (13,17,46,49). Nfia and Cd93 each had two potential miR-29 binding sites in the 3Ј-UTR segment analyzed, whereas Gpr85 had one site.…”
Section: Inhibition Of Mir-29 Activity Does Not Affect the Apoptosis mentioning
Background: miR-29 is a positive regulator of osteoblastogenesis, but its role in osteoclastogenesis is undefined. Results: Expression of all miR-29 family members increased during osteoclastic differentiation. miR-29 knockdown impaired migration, osteoclast commitment, and formation. Six novel miR-29 targets were identified. Conclusion: miR-29 promotes osteoclastogenesis. Significance: These data expand our understanding of osteoclastogenesis, providing insight into miR-29 function in hematopoietic cells and other lineages.
Tumors are presently a major threat to human life and health. Malignant tumors are conventionally treated through radiotherapy and chemotherapy. However, traditional therapies yield unsatisfactory results due to high toxicity to the normal cells, inability to treat deep tumor tissues, and the possibility of inducing drug resistance in the tumor cells. This has caused immunotherapy to emerge as an effective and alternate treatment strategy. To overcome the limitations of the conventional treatments as well as to avert the risk of various drug resistance and cytotoxicity, bacterial anti‐tumor immunotherapy has raised the interest of researchers. This therapeutic strategy employs bacteria to specifically target and colonize the tumor tissues with preferential accumulation and proliferation. Such bacterial accumulation initiates a series of anti‐tumor immune responses, effectively eliminating the tumor cells. This immunotherapy can use the bacteria alone or concomitantly with the other methods. For example, the bacteria can deliver the anti‐cancer effect mediators by regulating the expression of the bacterial genes or by synthesizing the bioengineered bacterial complexes. This review will discuss the mechanism of utilizing bacteria in treating tumors, especially in terms of immune mechanisms. This could help in better integrating the bacterial method with other treatment options, thereby, providing a more effective, reliable, and unique treatment therapy for tumors.
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