PubMed · 7523466
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
N P Burrows, R R Jones. 1994. Cell adhesion molecule expression in capillaritis.. https://doi.org/10.1016/s0190-9622(09)80060-1
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
Soluble DC-SIGN (CD209) bind unsialylated Lewis X epitopes that are abundantly expressed on neutrophils. Due to the low expression of unsialylated Lewis X epitopes on monocytes, no binding of soluble DC-SIGN molecules was seen. In contrast, beads coated with multiple DC-SIGN molecules show a high percentage of binding to monocytes. The increased number of DC-SIGN molecules present on the beads enable multivalent interactions between the DC-SIGN molecules and the scarce Lewis X epitopes present on monocytes. Increased expression of unsialylated Lewis X epitopes on monocytes after neuraminidase treatment coincided with enhanced binding to soluble DC-SIGN. Multiple unsialylated Lewis X epitopes in close proximity of each other are now able to interact multivalently to soluble DC-SIGN. From these findings, we conclude that firm interactions between DC-SIGN and monocytes can be established by either increasing the density of DC-SIGN molecules at the cell surface or by increasing the number of Lewis X epitopes. Regulating the number of ligands endows monocytes with the capacity to modulate binding to DC-SIGN. This may result in a bi-directional cross-talk between DC and monocytes, to modulate innate and/or adaptive immune responses.
Both eosinophil peroxidase (EPO) and neutrophil myeloperoxidase (MPO) preferentially oxidize SCN(-) to generate HOSCN, a weak, sulfhydryl-reactive oxidant, as a major physiologic product. We here show that HOSCN is a uniquely potent phagocyte oxidant inducer of E-selectin, ICAM-1, and VCAM-1 expression in HUVEC as detected by Western blot and flow cytometry. EMSA and inhibitor studies show that HOSCN up-regulation of these adhesion molecules is transcriptionally mediated through a mechanism that is dependent upon activation of the NF-kappaB p65/p50 transcription factor and constitutively suppressed by PI3K-Akt pathway activity. HUVEC monolayers exposed to HOSCN bind 8-fold more neutrophils and 3- to 4-fold more Aml14.3D10 cells (a differentiated cell line model of mature eosinophils) than control monolayers. Blocking Ab studies confirm the involvement of E-selectin and ICAM-1 but not VCAM-1 in neutrophil adhesion and of all three in Aml14.3D10 adhesion. Intraperitoneal injection of HOSCN evoked an 8-fold increase in neutrophil peritoneal extravasation. In addition to NF-kappaB, HOSCN also activates the potentially proinflammatory transcription factors Stat4, CDP, GRE, CBF, Ets-1/PEA3, and TFIID, a pattern easily distinguishable from that induced by LPS. These results suggest that phagocyte peroxidases function to amplify inflammation through a novel, HOSCN-specific oxidant mechanism.