China
Africa
Explore chapters and articles related to this topic
M cells and the follicle-associated epithelium
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Hiroshi Ohno, Marian Neutra, Ifor R. Williams
FAE cells differ from villus cells in their ability to release certain chemokines that attract immune cells toward the FAE and thus to sites of organized lymphoid tissue. In the small intestine of mice and humans, for example, chemokine CCL20, also designated macrophage inflammatory protein-3α (MIP-3α), is constitutively expressed in the FAE but not in the villus epithelium (Figure 15.2). CCL20 attracts subpopulations of DCs and lymphocytes that express the chemokine receptor CCR6. Mice that lack CCR6 have lower numbers of CD11c+ DCs in the subepithelial dome regions of Peyer's patches and have an impaired humoral immune response to orally administered antigen and certain enteropathogenic viruses. Cells of the mouse FAE also express CCL9 (analogous to CCL23 in humans), which attracts CCR1-expressing myeloid DCs, and CXCL16, which attracts CXCR6-expressing B and T lymphocytes into Peyer's patches.
Controlling Neuroinflammation
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
A model of experimental rabies has been set up in mice where intramuscular injection of a virulent strain of RABV into the hind limb, to mimic the bite given by a rabid animal, causes fatal encephalitis. Several studies performed in this mouse model, following the pattern of expression of inflammatory reagents (both genes and proteins), showed that in the nervous system, RABV infection triggers an innate immune response including chemokines (CCL5, CCL2, CCL9, and CXCL9), cyto-kines (IL-6 and IL-12), and IFN type I, as well as genes whose expression is regulated by IFN (Baloul et al. 2004; Camelo et al. 2000; Chopy et al. 2011 b; Sugiura et al. 2011; Wang et al. 2005). Analysis of expression of markers of inflammation by protein bioarrays showed that RABV stimulated the expression of 18 markers of inflammation (among the 40 present on the protein array) in the brains. The inflammatory markers were chemokines (CCL5, CCL2, CXCL11, and CXCL9), cytokines (IL-6, IL-12, and IL-13), and anti-inflammatory soluble proteins such as sTNFR1 and sTNFR2 interfering with the binding of TNF to its receptors (Chopy et al. 2011 b). The inflammatory reaction of the nervous system to RABV infection is transient with the expression of a majority of markers being rapidly down-regulated in the spinal cord and with a slight delay in the brain.
MicroRNA-mediated calcineurin signaling activation induces CCL2, CCL3, CCL5, IL8, and chemotactic activities in 4,4′-methylene diphenyl diisocyanate exposed macrophages
Published in Xenobiotica, 2021
Chen-Chung Lin, Brandon F. Law, Justin M. Hettick
A recent microarray-based study examining gene expression changes from lung tissues isolated from an MDI-OA murine model identified that chemokines, including Ccl6, Ccl8, Ccl9, Ccl11, Ccl12, Ccl17, and Ccl22, were among the most changed genes induced by MDI exposure (Wisnewski et al. 2020). Interestingly, our previous study identified that the chemokine signalling pathways were among the most enriched biological pathways that were targeted by both miR-206-3p and miR-381-3p (Lin et al. 2019), indicating that either miR-206-3p or miR-381-3p may participate in the regulation of chemokine expression and/or chemokine-induced signalling pathways. Our current results showed that CCL2, CCL3, CCL5, and CXCL8 transcription are induced by MDI-GSH conjugates through miR-206-3p and miR-381-3p mediated signalling pathways—potentially through calcineurin-mediated signalling activation in macrophages; it will be interesting to examine whether the same mechanism could apply to MDI-induced chemokines, such as CCL6, CCL8, CCL9, CCL11, CCL12, CCL17, and CCL22.
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.
MYC, MYCL, and MYCN as therapeutic targets in lung cancer
Published in Expert Opinion on Therapeutic Targets, 2020
Daniel Massó-Vallés, Marie-Eve Beaulieu, Laura Soucek
Two elegant studies recently expanded our understanding on the mechanism by which MYC instructs the immune system. In a NSCLC mouse model that co-expresses KRAS and MYC, Kortlever et al. showed that cooperation between these two oncogenes induced the formation of highly inflammatory and immune-suppressed tumors [158]. In this context, MYC was found to instruct profound changes not only in tumor cells, but also in the tumor microenvironment. Through expression of CCL9 and IL23, MYC promoted the recruitment of PD-L1-expressing CD206+ macrophages to the tumor stroma, alongside a reduction of tumor infiltrating lymphocytes (TILs), in particular CD3 + T cells, B220 + B cells, and Natural Killer (NK) cells. The latter were identified as crucial players in promoting tumorigenesis, since their depletion prevented tumor regression upon MYC deactivation. Intriguingly, neither CD4+ and CD8+ cell depletion nor PD-L1 blockade had an impact on these tumors [158].