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We propose and prove a family of generalized Lieb-Schultz-Mattis (LSM) theorems for symmetry protected topological (SPT) phases on boson/spin models in any dimensions. The "conventional" LSM theorem, applicable to e.g. any translation invariant system with an odd number of spin-1/2 particles per unit cell, forbids a symmetric short-range-entangled ground state in such a system. Here we focus on systems with no LSM anomaly, where global/crystalline symmetries and fractional spins within the unit cell ensure that any symmetric SRE ground state must be a nontrivial SPT phase with anomalous boundary excitations. Depending on models, they can be either strong or "higher-order" crystalline SPT phases, characterized by nontrivial surface/hinge/corner states. Furthermore, given the symmetry group and the spatial assignment of fractional spins, we are able to determine all possible SPT phases for a symmetric ground state, using the real space construction for SPT phases based on the spectral sequence of cohomology theory. We provide examples in one, two and three spatial dimensions, and discuss possible physical realization of these SPT phases based on condensation of topological excitations in fractionalized phases.

TIGIT, an immune checkpoint molecule widely expressed on NK cells, activated T cells and Tregs, has been involved in delivering inhibitory signals through the interaction with PVR. The blockade of TIGIT/PVR interaction is a promising approach in cancer immunotherapy. Here, we unexpectedly discovered the expression of TIGIT in murine tumor cells. To elucidate the mechanism of such intrinsic expression, TIGIT knockout murine colorectal CT26 and MC38 cell lines were generated by using CRISPR/Cas9 system. Although TIGIT knockout showed no effects on proliferation and colony formation of tumor cells in vitro , the tumor growth in mice was considerably inhibited. TIGIT knockout led to the increase of IFN-γ secretion by NK and CD8+ T cells. Further, in BABL/c nude mice, CD8+ T cells depleting mice and NK cells depleting nude mice, the promotion of tumor growth was significantly diminished, suggesting that both NK cells and CD8+ T cells were involved in the tumor promoting process mediated by intrinsic TIGIT. In addition, blocking TIGIT/PVR interaction by the antibody or recombinant PVR protein could elicit anti-tumor effects by facilitating the tumor infiltration and restoring the function of CD8+ T cells, and the antibody-mediate TIGIT blockade could inhibit MC38 tumor growth through blocking TIGIT expressed on tumor cells. We therefore propose a novel TIGIT/PVR interaction mode that tumor intrinsic TIGIT delivers inhibitory signals to CD8+ T cells and NK cells by engaging with PVR. [ABSTRACT FROM AUTHOR]

The extraction and characterization modified of type I collagen from rabbit-skins are investigated in this paper. Collagen was extracted from rabbit-skins by the combination of acid solubilization and pepsin solubilization. A qualitative analysis was carried out by SDS-PAGE. Both FT-IR and TG/DTG were employed to characterize the physical and chemical properties of the collagen. The results show that the extracted collagen is referred as type I collagen with a complete three-helix structure. In the process of thermal treatment, three stages of weight loss are observed at the temperatures of below 100 °C, between 200 °C and 450 °C, and after 450 °C, respectively. After being cross-linked by glutaraldehyde, the collagen was submitted to water content and enzyme degradation with I-collagenase in vitro. It is indicated that, after modification, the water content was (78. 7 it 1.3)%. The degradation rate decreases from (88. 65±0. 11)% to (6. 03 ±0.38)% (p<0. 01). Cytotoxicity of the modified collagen was evaluated by growth suppression technique (MTT chromatometry) against wild type mouse embryonic fibroblasts (MEF-WT). Its result shows that the cytotoxicity of the collagen is of grade 1 or grade 0, nearly no cytotoxicity. This collagen has a potential use in tissue engineering. [ABSTRACT FROM AUTHOR]

TIGIT, an immune checkpoint molecule widely expressed on NK cells, activated T cells and Tregs, has been involved in delivering inhibitory signals through the interaction with PVR. The blockade of TIGIT/PVR interaction is a promising approach in cancer immunotherapy. Here, we unexpectedly discovered the expression of TIGIT in murine tumor cells. To elucidate the mechanism of such intrinsic expression, TIGIT knockout murine colorectal CT26 and MC38 cell lines were generated by using CRISPR/Cas9 system. Although TIGIT knockout showed no effects on proliferation and colony formation of tumor cells in vitro , the tumor growth in mice was considerably inhibited. TIGIT knockout led to the increase of IFN-γ secretion by NK and CD8 + T cells. Further, in BABL/c nude mice, CD8 + T cells depleting mice and NK cells depleting nude mice, the promotion of tumor growth was significantly diminished, suggesting that both NK cells and CD8 + T cells were involved in the tumor promoting process mediated by intrinsic TIGIT. In addition, blocking TIGIT/PVR interaction by the antibody or recombinant PVR protein could elicit anti-tumor effects by facilitating the tumor infiltration and restoring the function of CD8 + T cells, and the antibody-mediate TIGIT blockade could inhibit MC38 tumor growth through blocking TIGIT expressed on tumor cells. We therefore propose a novel TIGIT/PVR interaction mode that tumor intrinsic TIGIT delivers inhibitory signals to CD8 + T cells and NK cells by engaging with PVR.

Overcoming drug-resistance is one of the major challenges to control tuberculosis (TB). The up-regulation of efflux pumps is one common mechanism that leads to drug-resistance. Therefore, immunotherapy targeting these efflux pump antigens could be promising strategy to be combined with current chemotherapy. Considering that CD8+ cytotoxic T lymphocytes (CTLs) induced by antigenic peptides (epitopes) could elicit HLA-restricted anti-TB immune response, efflux pumps from classical ABC family (Mycobacterium tuberculosis, Mtb) were chosen as target antigens to identify CTL epitopes. HLA-A2 restricted candidate peptides from Rv2937, Rv2686c and Rv2687c of Mycobacterium tuberculosis were predicted, synthesized and tested. Five peptides could induce IFN-γ release and cytotoxic activity in PBMCs from HLA-A2(+) PPD(+) donors. Results from HLA-A2/K(b) transgenic mice immunization assay suggested that four peptides Rv2937-p168, Rv2937-p266, Rv2686c-p151, and Rv2686c-p181 could induce significant CTL response in vivo. These results suggested that these novel epitopes could be used as immunotherapy candidates to TB drug-resistance.

Background and Objective: Protein 4.1, a component of cell membrane skeleton, plays a role in maintaining the shape and mechanical stability of erythrocytes. Recent researches showed that protein 4.1 may be associated with the development of tumors. This study was to investigate the expression and significance of membrane skeleton protein 4.1 family members (4.1B, 4.1R, 4.1N and 4.1G) in human non-small cell lung cancer (NSCLC)., Methods: The expression of proteins 4.1B, 4.1R, 4.1N and 4.1G in 147 specimens of NSCLC was detected by EnVision plus immunohistochemistry. The correlations of 4.1B, 4.1R, 4.1N and 4.1G expression to clinicopathologic features of NSCLC were analyzed by Wilcoxon rank sum test and Spearman rank correlation analysis., Results: The protein levels of 4.1B, 4.1R and 4.1N were significantly lower in lung squamous cell carcinoma tissues than in adjacent normal tissues (P<0.01). The protein levels of 4.1B, 4.1R, 4.1N and 4.1G were significantly lower in lung adenocarcinoma tissues than in adjacent normal tissues (P<0.05). The protein levels of 4.1B and 4.1G were significantly lower in lung squamous cell carcinoma tissues than in lung adenocarcinoma tissues (P<0.05). Protein 4.1G expression in squamous cell carcinoma was positively correlated to tumor cell differentiation (rs=0.386,P<0.01). In adenocarcinoma, the expression of proteins 4.1B, 4.1N and 4.1G were positively correlated to tumor cell differentiation (rs=0.276, P<0.05; rs=0.248,P<0.05; rs=0.268, P <0.05). The expression of protein 4.1s in squamous cell carcinoma and adenocarcinoma were not related to lymph node metastasis, tumor size, patients'age and sex (P>0.05)., Conclusions: Protein 4.1s are weakly expressed in NSCLC tissues than in adjacent normal tissues. The expression of proteins 4.1B, 4.1N and 4.1G are related to tumor cell differentiation.

Aim: To investigate if the nucleoside analogue lamivudine (LAM), a potent inhibitor of HBV replication, could restore the function of dendritic cells derived from patients with chronic hepatitis B (CHB) in an Asian population., Methods: Dendritic cells (DCs) derived from mononuclearcytes of patients with chronic HBV infection were cultured in the presence of IL-4, granulocyte-macrophage colony-stimulating factors (GM-CSF) and gradient concentrations of LAM (0-2 mmol/L). Cell morphology was observed under light microscopy. Cell surface molecules, including HLA-DR, CD80, CD83, and CD1alpha, were analyzed with flow cytometry. The concentrations of IL-6 and IL-12 in the supernatant were assayed by ELISA. T cell proliferation was assayed by methyl thiazolyl tetrazolium (MTT)., Results: The expression of CD1alpha on DC treated with 0.5 mmol/L LAM (LAM-DC 0.5 mmol/L) was significantly higher than that of DC untreated with LAM (54.1 +/- 4.21 vs 33.57 +/- 3.14, P < 0.05), and so was the expression of CD83 (20.24 +/- 2.51 vs 12.83 +/- 2.12, P < 0.05) as well as the expression of HLA-DR (74.5 +/- 5.16 vs 52.8 +/- 2.51, P < 0.05). Compared with control group, LAM-DC group (0.5 mmol/L) secreted significantly more IL-12 (910 +/- 91.5 vs 268 +/- 34.3 pg/mL, P < 0.05), had lower levels of IL-6 in the culture supernatant (28 +/- 2.6 vs 55 +/- 7.36 pg/mL, P < 0.05), markedly enhanced the stimulatory capacity in the allogeneic mixed leukocyte reaction (MLR) (1.87 +/- 0.6 vs 1.24 +/- 0.51, P < 0.05)., Conclusion: The lower expression of phenotypic molecules and impaired allogeneic mixed lymphocyte reaction function of dendritic cells derived from patients with HBV infection could be restored in vitro by incubation with LAM.

Background: Dendritic cells (DCs) loaded with complex antigen are always used to induce cytotoxic T lymphocytes (CTLs) which have a specific anti-tumor activity. However, CTLs can assault autologous cells induced by DCs loaded with autologous antigen. This study aimed to explore how to weaken the autoimmune reaction induced by DC vaccine by combining mature DC (mDC) activating immunity and immature DC (imDC) leading to immune tolerance to make hepatocellular carcinoma (HCC) vaccine in vitro., Methods: DC progenitors derived from human peripheral blood were assigned to two groups. One was cultured to mDC and pulsed with frozen-thawed antigen (FTA) of human HCC cell line SMMC-7721 cells (mDC group), and the other was cultured to imDC and pulsed with FTA of human liver cell line L-02 cells (imDC group). The morphology of DCs was monitored and cells phenotypes including HLA-DR, CD80, CD1alpha, CD83 were assayed by flowcytometry (FCM). The concentrations of interleukin-12 (IL-12) in the supernatant were assayed by ELISA. Methyl thiazolyl tetrazolium (MTT) was used to evaluate T cell proliferation induced by mDC and imDC and the killing rate of CTL induced by mDC and imDC respectively/together on SMMC-7721 and L-02 cells., Results: Compared with the imDC group, the mDC group was characterized by the following: increased secretion of IL-12 (P<0.05); higher expression of HLA-DR, CD1alpha, CD80, CD83; and stronger activity in stimulating proliferation of isogenic T cells (P<0.05). CTL induced by the mDC group had a significant killing response to SMMC-7721 as well as a higher killing rate for L-02 (P>0.05). CTL induced by mDC and imDC together had a higher killing response to SMMC-7721, but a lower killing rate for L-02 (P<0.01)., Conclusions: CTL induced by mDC and imDC together has a higher antigen-specific killing response in vitro than that induced by mDC alone. This may be of greater clinical value.

Aim: To study the effects of opioid receptor agonists endomorphin-1 and -2 on contractile responses of rat thoracic aorta rings to phenylephrine (PE) and angiotensin II (Ang II), and their possible mechanism in vitro., Methods: Isometric tension recording was progressed in thoracic aorta rings from Wistar rats., Results: Pretreatment of morphine, endomorphin-1 and -2 (0.1, 1, and 10 micromol/L) could inhibit the contractile responses of the endothelium-intact aorta rings to PE (0.1 micromol/L) and Ang II ( 1 micromol/L) in a concentration-dependent manner (P < 0.01), but could not inhibit the contraction of rings without endothelium (P > 0.05). Naloxone (1 micromol/L) could partially antagonize the effects of endomorphine-1 and -2 (P < 0.01). N(omega)-nitro-L-arginine (L-NNA, 10 micromol/L) or endothelial rubbing could completely blocked the effects of morphine, endomorphine-1 and -2 (P < 0.01)., Conclusion: Endomorphin-1 and -2 could inhibit PE- and Ang II-induced contractions of rat aorta rings, which was partially by naloxone-sensitive mechanism and related to the release of nitric oxide from vascular endothelium.