Monocyte-macrophages can be productively infected by CCR5-specific, but not CXCR4-specific, HIV-1. This could be due either to the absence of this chemokine receptor in this cell lineage or to other, yet undefined cellular cofactors that modulate the coreceptor activity of the CXCR4 in these cells. To investigate the basis of macrophage tropism, we studied the expression of CCR5 and CXCR4, as well as several of the other CC chemokine receptors, on monocyte-macrophages at different stages of differentiation. We found that on fresh monocytes, CXCR4 was relatively abundant, but it fell to barely detectable levels in culture over 24 hr and maintained this low level of expression during differentiation in vitro. Some donor macrophages appeared to express CXCR4 at levels comparable to CCR5. In contrast, CCR5 expression was low on fresh monocytes but increased on in vitro differentiation. Taken together, the results show that monocyte-macrophage differentiation is associated with a differential expression of chemokine receptors that may contribute to, but does not fully account for, the selectivity of these cells to HIV entry. GM-CSF, a cytokine that induces macrophage differentiation, caused a rapid decrease in CXCR4 and CCR5 mRNA and was correlated with decreased ability to support HIV entry.
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http://dx.doi.org/10.1089/aid.1998.14.129 | DOI Listing |
Front Immunol
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Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China.
CCL2, a pivotal cytokine within the chemokine family, functions by binding to its receptor CCR2. The CCL2/CCR2 signaling pathway plays a crucial role in the development of fibrosis across multiple organ systems by modulating the recruitment and activation of immune cells, which in turn influences the progression of fibrotic diseases in the liver, intestines, pancreas, heart, lungs, kidneys, and other organs. This paper introduces the biological functions of CCL2 and CCR2, highlighting their similarities and differences concerning fibrotic disorders in various organ systems, and reviews recent progress in the diagnosis and treatment of clinical fibrotic diseases linked to the CCL2/CCR2 signaling pathway.
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Department of Medical Microbiology and Infection Prevention, Amsterdam UMC location University of Amsterdam, Amsterdam, the Netherlands.
Atopic dermatitis (AD) is characterized by dysregulated T cell immunity and skin microbiome dysbiosis with predominance of Staphylococcus aureus, which is associated with exacerbating AD skin inflammation. Specific glycosylation patterns of S. aureus cell wall structures amplify skin inflammation through interaction with Langerhans cells (LCs).
View Article and Find Full Text PDFNat Cancer
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Center for Cancer Research, Medical University of Vienna, Comprehensive Cancer Center, Vienna, Austria.
Dendritic cell (DC) activation by pattern recognition receptors like Toll-like-receptors (TLRs) is crucial for cancer immunotherapies. Here, we demonstrate the effectiveness of the TLR7/8 agonist imiquimod (IMQ) in treating both local tumors and distant metastases. Administered orally, IMQ activates plasmacytoid DCs (pDCs) to produce systemic type I interferons (IFN-I) required for TLR7/8 upregulation in DCs and macrophages, sensitizing them to topical IMQ treatment, which is essential for therapeutic efficacy.
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Hangzhou Lin'an Traditional Chinese Medicine Hospital, Affiliated Hospital, Hangzhou City University, Hangzhou, China.
Golgi Protein 73 (GP73) is a Golgi-resident protein that is highly expressed in primary tumor tissues. Initially identified as an oncoprotein, GP73 has been shown to promote tumor development, particularly by mediating the transport of proteins related to epithelial-mesenchymal transition (EMT), thus facilitating tumor cell EMT. Though our previous review has summarized the functional roles of GP73 in intracellular signal transduction and its various mechanisms in promoting EMT, recent studies have revealed that GP73 plays a crucial role in regulating the tumor and immune microenvironment.
View Article and Find Full Text PDFNat Commun
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Department of Neuroscience, Center for Brain Immunology and Glia, University of Virginia School of Medicine, Charlottesville, VA, USA.
Microglia and the border-associated macrophages contribute to the modulation of cerebral blood flow, but the mechanisms have remained uncertain. Here, we show that microglia regulate the cerebral blood flow baseline and the responses to whisker stimulation or intra-cisternal magna injection of adenosine triphosphate, but not intra-cisternal magna injection of adenosine in mice model. Notably, microglia repopulation corrects these cerebral blood flow anomalies.
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