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Acute and chronic venous thrombosis: Pathogenesis and new insights
Published in Peter Gloviczki, Michael C. Dalsing, Bo Eklöf, Fedor Lurie, Thomas W. Wakefield, Monika L. Gloviczki, Handbook of Venous and Lymphatic Disorders, 2017
Jose A. Diaz, Thomas W. Wakefield, Peter K. Henke
P-selectin is a critical adhesion molecule involved in the interactions between inflammatory cells and vessels, and has been linked with cardiovascular events in both the arterial and the venous circulations.24 This molecule is present in the α-granules of platelets and the Weibel–Palade bodies of endothelial cells. It is first translocated to the plasma membrane of these cells, mediating the initial inflammatory response.25 Recombinant soluble P-selectin glycoprotein ligand-Ig (rPSGL-Ig) binds and inhibits cell-associated P-selectin. Thrombin-activated platelets expressing P-selectin bind to neutrophils, and rPSGL-Ig blocks this effect by approximately 90%.26 Recently, a synergism between leukocytes and platelets has been identified,27 such that TF can be transferred from leukocytes to platelets in a P-selectin-mediated fashion, and even platelets have been demonstrated to express functional PSGL-1, allowing for a P-selectin mechanism for platelet rolling (Figure 8.3c).28,29
Lymphocyte homing and immunology of extranodal lymphoid tissues
Published in Franco Cavalli, Harald Stein, Emanuele Zucca, Extranodal Lymphomas, 2008
Mariagrazia Uguccioni, James J Campbell, Katrin Kuscher, Marshall E Kadin
The intestinal lamina propria (LP) contains numerous previously activated/memory CD4+ T-cells involved in intestinal immunity and the induction and maintenance of chronic intestinal inflammation.41 T-cell entry into the intestinal mucosa is mediated by distinct sets of cell adhesion molecules expressed on the T-cell and intestinal microvascular endothelial surface. Interaction between the gut-associated integrin α4β7, on the T cell surface, with its ligand MAdCAM-1, on intestinal microvascular endothelium cells, is important for T-cell entry into the LP.42–44 Moreover, antibody neutralization studies suggest a role for P-selectin and P-selectin glycoprotein ligand 1 (PSGL-1) in effector CD4+ T-cell entry to this site. The chemokine receptor CCR9 is required for efficient effector CD8+ T-cell localization to the small intestinal epithelium.40,45
Mast Cell Activation and Leukocyte Recruitment Responses Into Skin Sites
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Michael D. Ioffreda, George F. Murphy
Neutrophil slowing within venules, also known as margination, involves neutrophil rolling along the lumenal endothelial surface at velocities of less than 50 μm/sec (36), and is moderated by CAMs belonging to the selectin family. Members of the selectin family have in common an N-terminal, lectin-like domain capable of binding specific carbohydrate ligands on leukocytes (37). L-selectin (LECAM-1) is constitutively expressed on the surface of neutrophils and loosely binds them to endothelial cells via an as yet unidentified ligand. P-selectin (CD62, GMP140, PADGEM) mediates relatively weak, rolling adhesion between leukocytes and endothelial cells under flow conditions. It is constitutively stored in cytoplasmic, lysosome-like Weibel-Palade bodies and is translocated to the lumenal endothelial surface within minutes of exposure to histamine, thrombin, bradykinin, leukotriene C4, or free radicals (38). Mast cells may be the direct source of histamine and leukotriene C4, which contribute to P-selectin-mediated rolling of neutrophils on postcapillary venules (39,40). The ligand for P-selectin on neutrophils may be P-selectin glycoprotein ligand (PSGL-1) (41). The binding interaction between neutrophils and E-selectin is capable of supporting neutrophil rolling under conditions of flow in vitro, suggesting that E-selectin expressed by cutaneous vessels could potentially contribute to neutrophil rolling in vivo (42). It is expressed by postcapillary venules (43) in response to TNF-α, which is produced and secreted by a variety of skin cell types, including mast cells (Fig. 1E). Indeed, mast cell degranulation is known to directly up-regulate expression of E-selectin in a TNF-α-dependent manner (9,44).
Inflammation-targeted cannabidiol-loaded nanomicelles for enhanced oral mucositis treatment
Published in Drug Delivery, 2022
Yingke Liu, Xingying Qi, Yashi Wang, Man Li, Quan Yuan, Zhihe Zhao
To further evaluate the inflammation degree, the presence of Ly6G cells, which include polymorphonuclear neutrophils or polymorphonuclear myeloid-derived suppressor cells (MDSCs), was assessed by Ly6G staining. Normal tongue tissue served as control, where no Ly6G cell infiltration was observed (Supplementary Figure S5). Compared to PBS and free CBD, CBD/FD nanomicelles significantly reduced Ly6G cell infiltration, exhibiting an improved anti-inflammatory effect. (Figure 6(A)). The interaction of P-selectin glycoprotein ligand 1 (PSGL-1) expressed on Ly6G + cells and P-selectin expressed on vascular endothelial cells mediated the process of cell infiltration. Therefore, we speculate that the reduced infiltration of Ly6G cells is partly due to the ability of fucoidan competitively bind to P-selectin. It is analogous to how low-molecular-weight heparin can competitively bind P-selectin and thereby inhibits the recruitment of MDSCs (Stadtmann et al., 2013; Long et al., 2020).
Release of α-granule contents during platelet activation
Published in Platelets, 2022
Platelets are the major source of soluble P-selectin, which is shed from their surface following activation. Although the exact mechanism remains unknown it has been suggested interaction with its receptor PSGL-1 on leukocytes is required for P–selectin shedding [146–149]. Additionally, platelets also express and release a splice variant of P-selectin which lacks the transmembrane region, however this is only responsible for a minor portion of soluble P-selectin [126,150,151]. Although soluble P-selectin can also be derived from endothelial cells, strong correlation with platelet count has been shown [125,126,152]. Provided plasma is immediately separated from cellular component of blood, soluble P-selectin is resistant to ex vivo platelet activation and additionally not influenced by differing anticoagulation or plasma preparation making it a reliable marker [153].
Recent advances in the understanding of enterovirus A71 infection: a focus on neuropathogenesis
Published in Expert Review of Anti-infective Therapy, 2021
Han Kang Tee, Mohd Izwan Zainol, I-Ching Sam, Yoke Fun Chan
PSGL-1 is a sialomucin leukocyte membrane protein that functions as a ligand for selectins [58]. It is expressed as a homodimer of disulfide-linked subunits. It is mainly located on most of the circulating myeloid cells (including neutrophils, monocytes, and most lymphocytes) and even retained after extravasation into tissues [59]. Other than myeloid cells, it is also expressed on dendritic cells and macrophages in intestinal mucosa. A study has shown that Jurkat T cells support EV-A71 infection via a PSGL-1-dependent manner, with the VP1-145 residue of EV-A71 mediating PSGL-1 binding [60]. However, human PSGL-1 expression in transgenic mice failed to enhance EV-A71 infectivity, implying that PSGL-1 alone is not sufficient to induce lethality in mice [61]. A comparative study analyzing both SCARB2 and PSGL-1 further demonstrated that PSGL-1 is unable to induce EV-A71 uncoating [52].