Immunomodulatory Function of Pien Tze Huang in T Cell-Mediated Anti-tumor Activity against B16-F10, MC38 and Hep1-6 Tumor Models.

Objective: To investigate the anti-tumor effects of Pien Tze Huang (PZH) in mouse models of B16-F10 melanoma, MC38 colorectal cancer, Hep1-6 hepatocellular carcinoma and chemically induced hepatocellular carcinoma model.

Methods: Various tumor models, including B16-F10, MC38 and Hep1-6 tumor hypodermic inoculation models, B16-F10 and Hep1-6 pulmonary metastasis models, Hep1-6 orthotopic implantation model, and chemically induced hepatocellular carcinoma model, were utilized to evaluate the anti-tumor function of PZH. Tumor growth was assessed by measuring tumor size and weight of solid tumors isolated from C57BL/6 mice.

MHC class II regulation of CD8 T cell tolerance and implications in autoimmunity and cancer immunotherapy.

Major histocompatibility complex (MHC) class II-reactive CD8 T cells are found in humans and animals, but little is known about their identity, development, and function. In this study, we discover a group of CD8 T cells reactive to both MHC class I and II molecules in MHC class II-deficient mice. We clone their T cell receptors (TCRs) and analyze their development and function.

The miR-17∼92 miRNAs promote plasma cell differentiation by suppressing SOCS3-mediated NIK degradation.

The miR-17∼92 family microRNAs (miRNAs) play a key role in germinal center (GC) reaction through promoting T follicular helper (T) cell differentiation. It remains unclear whether they also have intrinsic functions in B cell differentiation and function. Here we show that mice with B cell-specific deletion of the miR-17∼92 family exhibit impaired GC reaction, plasma cell differentiation, and antibody production in response to protein antigen immunization and chronic viral infection.

Glycogen synthase kinase 3 controls T-cell exhaustion by regulating NFAT activation.

Cellular immunity mediated by CD8 T cells plays an indispensable role in bacterial and viral clearance and cancers. However, persistent antigen stimulation of CD8 T cells leads to an exhausted or dysfunctional cellular state characterized by the loss of effector function and high expression of inhibitory receptors during chronic viral infection and in tumors. Numerous studies have shown that glycogen synthase kinase 3 (GSK3) controls the function and development of immune cells, but whether GSK3 affects CD8 T cells is not clearly elucidated.

Sulfate oligosaccharide of Gracilaria lemaneiformis modulates type 1 immunity by restraining T cell activation.

Seaweeds are important "blue food" and some seaweeds have been demonstrated that have the immunoregulation activities and benefit for human health. However, which immune cell subsets are targeted and how immune processes are regulated by those seaweeds remain poorly understood. Here we identified sulfated oligosaccharide of Gracilaria lemaneiformis (GLSO) inhibits IFNγ production by T cells in ovalbumin (OVA) immunized mice and in vitro activation system of OVA-specific CD4 T cells.

Are the Derived Indexes of Peripheral Whole Blood Cell Counts (NLR, PLR, LMR/MLR) Clinically Significant Prognostic Biomarkers in Multiple Myeloma? A Systematic Review And Meta-Analysis.

Background: Multiple myeloma (MM) is an incurable malignant plasma cell tumor. Whole blood cell count (WBCC) derived indexes are widely used as a predictive biomarker for various types of solid and hematological malignant tumors. Our study is to evaluate its effectiveness in MM by meta-analysis.

Glycogen synthase kinase 3 drives thymocyte egress by suppressing β-catenin activation of Akt.

Molecular pathways controlling emigration of mature thymocytes from thymus to the periphery remain incompletely understood. Here, we show that T cell–specific ablation of glycogen synthase kinase 3 (GSK3) led to severely impaired thymic egress. In the absence of GSK3, β-catenin accumulated in the cytoplasm, where it associated with and activated Akt, leading to phosphorylation and degradation of Foxo1 and downregulation of Klf2 and S1P expression, thereby preventing emigration of thymocytes.