CCL21-Ser expression in melanoma cells recruits CCR7+ naïve T cells to tumor tissues and promotes tumor growth.

CCL21-Ser, a chemokine encoded by the Ccl21a gene, is constitutively expressed in the thymic epithelial cells and stromal cells of secondary lymphoid organs. It regulates immune cell migration and survival through its receptor CCR7. Herein, using CCL21-Ser-expressing melanoma cells and the Ccl21a-deficient mice, we demonstrated the functional role of cancer cell-derived CCL21-Ser in melanoma growth in vivo. The B16-F10 tumor growth was significantly decreased in Ccl21a-deficient mice compared with that in wild-type mice, indicating that host-derived CCL21-Ser contributes to melanoma proliferation in vivo. In Ccl21a-deficient mice, tumor growth of melanoma cells expressing CCL21-Ser was significantly enhanced, suggesting that CCL21-Ser from melanoma cells promotes tumor growth in the absence of host-derived CCL21-Ser. The increase in tumor growth was associated with an increase in the CCR7+ CD62L+ T cell frequency in the tumor tissue but was inversely correlated with Treg frequency, suggesting that naïve T cells primarily promote tumor growth. Adoptive transfer experiments demonstrated that naïve T cells are preferentially recruited from the blood into tumors with melanoma cell-derived CCL21-Ser expression. These results suggest that CCL21-Ser from melanoma cells promotes the infiltration of CCR7+ naïve T cells into the tumor tissues and creates a tumor microenvironment favorable for melanoma growth.

Enhanced Ag(+) Ion Release from Aqueous Nanosilver Suspensions by Absorption of Ambient CO2.

Nanosilver with closely controlled average particle diameter (7-30 nm) immobilized on nanosilica is prepared and characterized by X-ray diffraction, N2 adsorption, and transmission electron microscopy. The presence of Ag2O on the as-prepared nanosilver surface is confirmed by UV-vis spectroscopy and quantified by thermogravimetric analysis and mass spectrometry. The release of Ag(+) ions in deionized water is monitored electrochemically and traced quantitatively to the dissolution of a preexisting Ag2O monolayer on the nanosilver surface. During this dissolution, the pH of the host solution rapidly increases, suppressing dissolution of the remaining metallic Ag. When, however, a nanosilver suspension is exposed to a CO2-containing atmosphere, like ambient air during its storage or usage, then CO2 is absorbed by the host solution decreasing its pH and contributing to metallic Ag dissolution and further leaching of Ag(+) ions. So the release of Ag(+) ions from the above closely sized nanosilver solutions in the absence and presence of CO2 as well as under synthetic air containing 200-1800 ppm of CO2 is investigated along with the solution pH and related to the antibacterial activity of nanosilver.

Endogenous CCL21-Ser deficiency reduces B16-F10 melanoma growth by enhanced antitumor immunity.

The chemokine CCL21 regulates immune and cancer cell migration through its receptor CCR7. The Ccl21a gene encodes the isoform CCL21-Ser, predominantly expressed in the thymic medulla and the secondary lymphoid tissues. This study examined the roles of CCL21-Ser in the antitumor immune response in Ccl21a-knockout (KO) mice. The Ccl21a-KO mice showed significantly decreased growth of B16-F10 and YUMM1.7 melanomas and increased growth of MC38 colon cancer, despite no significant difference in LLC lung cancer and EO771 breast cancer. The B16-F10 tumor in Ccl21a-KO mice showed melanoma-specific activated CD8+ T cell and NK cell infiltration and higher Treg counts than wild-type mice. B16-F10 tumors in Ccl21a-KO mice showed a reduction in the positive correlation between the ratio of regulatory T cells (Tregs) to activated CD8+ T cells and tumor weight. In Ccl21a-KO tumor, the intratumoral Tregs showed lower co-inhibitory receptors TIM-3 and TIGIT. Taken together, these results suggest that endogenous CCL21-Ser supports melanoma growth in vivo by maintaining Treg function and suppressing antitumor immunity by CD8+ T cells.

Superior catalytic performance of intermetallic CaPt2 nanoparticles supported on titanium group oxides in hydrogenation of ketones to alcohols.

Intermetallic CaPt2 nanoparticles, supported on titanium group oxides, were prepared using a molten salt method with CaH2 as both the reducing agent and the calcium source. The nanoparticles exhibited superior catalytic activity compared to a commercial Pt/C catalyst in the hydrogenation of ketones to alcohols, which could be promoted by electron-rich Pt sites in CaPt2.