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Inflammation and spermatogenesis
Published in C. Yan Cheng, Spermatogenesis, 2018
Maria Susana Theas, Patricia Verónica Jacobo, Cecilia Valeria Pérez, Vanesa Anabella Guazzone, Livia Lustig
Macrophages also play the role of antigen-presenting cells and release inflammatory cytokines and chemokines that contribute to EAO development. In fact, in vivo depletion of these cells with clodronate-containing liposomes in rats undergoing EAO decreased incidence and severity of testicular damage. Testicular macrophage population is heterogeneous; it includes resident macrophages (ED2+ cells), inflammatory monocytes recently arrived from circulation (ED1+ cells), and double-positive (ED1+ ED2+) subpopulation, the major contributor to the macrophage number increase in EAO.46 Inflammatory chemokines CCL2, CCL3, and CCL4 regulate macrophage recruitment within the interstitium via CCR2, CCR1, and CCR5 receptors.47–49
Cell Recruitment for Intervertebral Disc
Published in Raquel M. Gonçalves, Mário Adolfo Barbosa, Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
Catarina Leite Pereira, Sibylle Grad, Mário Adolfo Barbosa, Raquel M. Gonçalves
CCL3, also known as macrophage inflammatory protein (MIP)-1α, was shown to be upregulated in NP cells isolated from rat and human IVD tissue following treatment with IL-1β or TNF-α. In the same study, CCL3 expression in human samples was shown to be correlated with the grade of tissue degeneration (Wang et al. 2013). This molecule induced macrophage migration after treatment with NP cells conditioned media (previously treated with IL-1β or TNF-α); migration was suggested to occur via CCR1, the primary receptor of CCL3, since its inhibition resulted in cell migration blockage (Wang et al. 2013). CCL2 and CCL3 gene expression were shown to be significantly up-regulated in both human AF and NP cells after treatment with IL-1β (Liu et al. 2017b; Wang et al. 2013). Additionally, some of those chemokines, such as CCL2, CCL7, and CXCL18, have been correlated with histological degenerative tissue changes (Phillips et al. 2013) and are known to be involved in the recruitment of immune cells to inflammatory sites (Luster 1998).
Pseudomyxoma peritonei
Published in Wim P. Ceelen, Edward A. Levine, Intraperitoneal Cancer Therapy, 2015
Residual disease following CRS was scored according to the CCR score [48]. CCR0 indicates no macroscopic residual cancer; CCR1 indicates no residual nodule larger than 2.5 mm in diameter; CCR2 indicates residual nodules between 2.5 mm and 2.5 cm in diameter; and CCR3 implies residual disease greater than 2.5 cm in diameter. Overall CC0 and CC1 equate to a complete cytoreduction with optimal outcomes and significantly better than patients who have CCR2 or CCR3 cytoreduction.
Association between cytokines and exosomes in synovial fluid of individuals with knee osteoarthritis
Published in Modern Rheumatology, 2020
Kun Gao, Wenxiu Zhu, Heng Li, Dujun Ma, Weidong Liu, Weiji Yu, Lixin Wang, Yafei Cao, Yong Jiang
The reasons why SF-derived exosomes can influence lymphocytes and chondrocytes needs intensive exploration. IL-1β and TNF-α have been reported to induce apoptosis when exposed to chondrocytes [15,25,26]. CCR1 and CCR5 are the chemokine receptors of CCL3, CCL4, CCL5, CCL6, CCL9, CCL10, and CCL15. They are highly expressed in macrophages and have been proven to be able to recruit monocytes and T cells [27–29]. CCL2, CXCL8, and CXCL1 have been reported to express elevated levels in KOA. CXCL1 stimulation can initiate the apoptosis of chondrocytes [11]. MCP-1/CCL2 can decrease proteoglycan synthesis in OA chondrocytes and initiate the release of MMP-3, MMP-13 and NAG. CXCL8/IL-8 and CXCL11 can inhibit the proliferation of chondrocytes, promote the apoptosis of chondrocytes, and stimulate chondrocytes to secrete a variety of cytokines that promote inflammatory responses [3,13]. Since many cytokines have influence on cell migration and inflammation, it is hard to identify the most active ones. Exosomes can preserve cytokines for a long period of time and target specific cells, and therefore they definitely have a significant impact on the inner environment of KOA.
Rapid identification of highly potent human anti-GPCR antagonist monoclonal antibodies
Published in mAbs, 2020
Martin J. Scott, Amanda Jowett, Martin Orecchia, Peter Ertl, Larissa Ouro-Gnao, Julia Ticehurst, David Gower, John Yates, Katie Poulton, Carol Harris, Michael J. Mullin, Kathrine J. Smith, Alan P. Lewis, Nick Barton, Michael L. Washburn, Ruud de Wildt
Although in vivo immunization approaches have been exemplified for diverse GPCR targets,3,19,31,33,40,41 we wanted to assess the utility of an in vitro yeast-based discovery platform (AdimabTM), comprising large and diverse libraries of human mAbs, and magnetic-activated cell sorting (MACS®) selections to isolate target binders in order to reduce lead discovery timelines. We selected a GPCR of therapeutic relevance (CCR1, a class A chemokine receptor) for these investigations. With concerns over limited epitope diversity using linear peptide antigens based on the exposed CCR1 N-terminus, and without the availability of purified recombinant hCCR1 at the time of initiating these efforts, we instead compared two readily available ‘membrane-associated’ antigen formats over-expressing the target of interest, specifically, CHO-hCCR1 cells and hCCR1 VLPs.
Immunobiology of periprosthetic inflammation and pain following ultra-high-molecular-weight-polyethylene wear debris in the lumbar spine
Published in Expert Review of Clinical Immunology, 2018
John H. Werner, John H. Rosenberg, Kristen L. Keeley, Devendra K. Agrawal
Alternatively, Gibon et al [61] determined that MSC recruitment is driven in part by CCR1 signaling in response to UHMWPE wear debris. The group had previously demonstrated that CCR1 is involved in recruiting macrophages and MSCs in response to polymethylmethacrylate (PMMA) particles [70]. CCR1 is a chemokine receptor that promotes recruitment of macrophages and MSCs. CCR1 receptor antagonism disrupts the ability of MSCs to respond to UHMWPE debris. This impairs the ability of MSCs to balance the osteolytic process, leading to greater bone resorption [61]. Chemokine pathways are vital for recruitment of inflammatory and regenerative cell populations. Therapies aimed at modulating these pathways may improve management of peri-implant inflammation (Figure 1). Development of drug-releasing implants for local administration of chemokine modulators could avoid systemic side effects and increase efficacy [64,66]. Macrophage and MSC recruitment to wear particle debris is complex, and various chemokines are involved. Combination treatment targeting multiple chemokine pathways may achieve optimal osteolysis prevention.