No abstract

We report on an efficient method for the formation of modified cellulose-based materials with enhanced hydrophobic properties, formed by grafting with polymeric epoxidized soybean oil (ESO) as a renewable, environmentally friendly, and low cost raw material. The grafting process occurred via ring-opening polymerization, wherein the cellulose hydroxyl groups acted as initiators in the presence of a SnCl 4 catalyst, linking the cellulose fibers and ESO via ether linkages, thereby forming a polymeric matrix. The surface polarity was therefore decreased by the substitution of cellulose hydroxyl groups for long-chain hydrophobic alkane moieties from ESO. The water contact angle of modified filter paper reached 145.1°w ith the surface free energy decreasing to 22.07 mJ m −2 and a hydration free energy of −13.09 mJ m −2 . The presence of polymeric ESO nanoparticles on the modified cellulose fibers suggested that the hydrophobicity was not only dependent on the surface composition but was also closely related to the surface morphology. To reveal the effects of surface morphology on hydrophobicity, smooth cellulose films anchored to mica plates via PVAm with a surface roughness of 1.698 nm were prepared by spin coating and modified with ESO. The thus-formed modified cellulose films also contained polymeric ESO nanoparticles which increased their roughness and enhanced their hydrophobic properties.

The CD4 ؉ CD25 ؉ FOXP3 ؉ regulatory T (Treg) cells are critical for maintaining immune tolerance in healthy individuals and are reported to restrict anti-inflammatory responses and thereby promote tumor progression, suggesting them as a target in the development of antitumor immunotherapy. Forkhead box P3 (FOXP3) is a key transcription factor governing Treg lineage differentiation and their immune-suppressive function. Here, using Treg cells, as well as HEK-293T and Jurkat T cells, we report that the stability of FOXP3 is directly and positively regulated by the E3 ubiquitin ligase ring finger protein 31 (RNF31), which catalyzes the conjugation of atypical ubiquitin chains to the FOXP3 protein. We observed that shRNA-mediated RNF31 knockdown in human Treg cells decreases FOXP3 protein levels and increases levels of interferon-␥, resulting in a Th1 helper cell-like phenotype. Human Treg cells that ectopically expressed RNF31 displayed stronger immune-suppressive capacity, suggesting that RNF31 positively regulates both FOXP3 stability and Treg cell function. Moreover, we found that RNF31 is up-regulated in Treg cells that infiltrate human gastric tumor tissues compared with their counterparts residing in peripheral and normal tissue. We also found that elevated RNF31 expression in intratumoral Treg cells is associated with poor survival of gastric cancer patients, suggesting that RNF31 supports the immune-suppressive functions of Treg cells. Our results suggest that RNF31 could be a potential therapeutic target in immunity-based interventions against human gastric cancer.