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The wintertime variations and distributions of sea surface temperature (SST) and thermal fronts associated with the spatial distribution of ichthyoplankton were investigated in the continental shelf waters of the southern East China Sea (ECS) by using 10 year (2005-2015) satellite SST images with an entropy-based edge detection method. The Mainland China Coastal Front and Kuroshio Front (KF) in winter (December to March) were examined with SST gradient magnitudes (GMs) of 0.20-0.40 and 0.30-0.45°C Km−1, respectively, along the 50 m and 100-200 m isobaths in the southern ECS. These two fronts coincided with isotherms of 14-16°C and 21-22°C, respectively. The Mainland China Coastal Front pattern remained fairly stable along the 50 m isobaths, and the coexisting SST front and upwelling were shifted seaward or shoreward with the recession or intrusion of the KF during the winters. Notably, the SST GMs of the KF showed a significant strengthening that was higher than those of the past two decades. Moreover, the total abundance of the nearshore waters of the KF (which was occupied by approximately 75% neritic species) was 23 times higher than that of the offshore waters (which was occupied by approximately 63.60% oceanic species). We suggest that the generation of the KF in winter may act as the biological barrier of oceanic organisms and larval fishes in the study area. [ABSTRACT FROM AUTHOR]

Antitumor cytotoxic T lymphocytes (CTLs) are essential for immune surveillance, yet the blockade of eliciting such CTLs during oncolytic virotherapy remains incompletely understood. Here, we show that oncolysis of mesothelioma by modified vaccinia Tiantan (MVTT) induces damage-associated molecular patterns exposure. Although MVTT leads to regression of established mesothelioma dose-dependently, antitumor CTLs are rarely induced. Mechanistically, MVTT virotherapy generates C-X-C chemokines that recruit CXCR2-expressing polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) into tumor microenvironment, where they suppress dendritic cells (DCs) by producing IL-10 and halt CTL responses. During the virotherapy, however, depletion of PMN-MDSCs but not of monocytic (M)-MDSCs results in the induction of potent antitumor CTLs that not only eradicate established mesothelioma but also prevent the second tumor challenge. Our findings suggest that vaccinia virotherapy may combine strategies that prevent the chemotactic recruitment of PMN-MDSCs, block their suppression on DCs or deplete PMN-MDSCs in order to induce potent CTLs for tumor eradication. [ABSTRACT FROM AUTHOR]