Compared to RGB semantic segmentation, RGBD semantic segmentation can achieve better performance by taking depth information into consideration. However, it is still problematic for contemporary segmenters to effectively exploit RGBD information since the feature distributions of RGB and depth (D) images vary significantly in different scenes. In this paper, we propose an Attention Complementary Network (ACNet) that selectively gathers features from RGB and depth branches. The main contributions lie in the Attention Complementary Module (ACM) and the architecture with three parallel branches. More precisely, ACM is a channel attention-based module that extracts weighted features from RGB and depth branches. The architecture preserves the inference of the original RGB and depth branches, and enables the fusion branch at the same time. Based on the above structures, ACNet is capable of exploiting more high-quality features from different channels. We evaluate our model on SUN-RGBD and NYUDv2 datasets, and prove that our model outperforms state-of-the-art methods. In particular, a mIoU score of 48.3% on NYUDv2 test set is achieved with ResNet50. We will release our source code based on PyTorch and the trained segmentation model at https://github.com/anheidelonghu/ACNet.

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Tumor-associated macrophages are a prominent component of lung cancer stroma and contribute to tumor progression. The protein V-set and Ig domain-containing 4 (VSIG4), a novel B7 family-related macrophage protein that has the capacity to inhibit T-cell activation, has a potential role in the development of lung cancer. In this study, 10 human non-small-cell lung cancer specimens were collected and immunohistochemically analyzed for VSIG4 expression. Results showed massive VSIG4 þ cell infiltration throughout the samples. Immunofluorescent double staining showed that VSIG4 was present on CD68 þ macrophages, but absent from CD3 þ T cells, CD31 þ endothelial cells, and CK-18 þ epithelial cells. Moreover, VSIG4 was coexpressed on B7-H1 þ and B7-H3 þ cells in these tumor specimens. Transfection of the VSIG4 gene into 293FT cells demonstrated that the VSIG4 signal could inhibit cocultured CD4 þ and CD8 þ T-cell proliferation and cytokine (IL-2 and IFN-g) production in vitro. Interestingly, in a murine tumor model induced by Lewis lung carcinoma cell line, we found that tumors grown in VSIG4-deficient (VSIG4 À / À ) mice were significantly smaller than those found in wildtype littermates. All of these results demonstrate that macrophage-associated VSIG4 is an activator that facilitates lung carcinoma development. Specific targeting of VSIG4 may prove to be a novel, efficacious strategy for the treatment of this carcinoma.

VSIG4 controls inflammation through MS4A6D-mediated transcriptional inhibition of Nlrp3 and Il-1β in macrophages.

BTLA promotes the pathogenesis of virus-induced FH by enhancing macrophage viability and function. Targeting BTLA may be a novel strategy for the treatment of FH.

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Chronic hepatitis B was characterized by fluctuant immune response to infected hepatocytes resulting in hepatic inflammation and virus persistence. Recently, Programmed Death-1 (PD-1) and its ligand PD-L1 have been demonstrated to play an essential role in balancing antiviral immunity and inflammation in the livers of acute hepatitis B patients, significantly influencing disease outcome. PD-1 up-regulation in peripheral T cells is associated with immune dysfunction in chronic hepatitis B patients. However, the effect of PD-1/PD-L1 on hepatic damage and chronic infective status is still unknown in patients with chronic HBV infection. Here, we report up-regulation of PD-1 and PD-L1 in liver biopsies from 32 chronic HBV patients compared to 4 healthy donors. PD-1/PD-L1 up-regulation was significantly associated with hepatic inflammation and ALT elevation. Moreover, appropriate up-regulation but not overexpression of PD-L1 in the active phase of chronic hepatitis B as well as lower expression of PD-L1 in the inactive phase in liver residential antigen presenting cells (including Kupffer cells and sinusoidal endothelial cells) may contribute to viral inhibition. Our data suggest that the intrahepatic interaction of PD-1 and PD-L1 might play an important role in balancing the immune response to HBV and immune-mediated liver damage in chronic HBV infection.

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