Long-term CXCR3 antagonist AMG487 mitigated acute graft-versus-host disease by inhibiting T cell activation in a murine model.

Background: Lymphocyte migration plays a key role in the development of acute graft-versus-host disease (aGVHD). Blocking lymphocyte migration by targeting chemokine receptors, such as CXCR3, may be a promising strategy for preventing and treating aGVHD. Our previous studies have shown that short-term CXCR3 antagonist treatment combined with cyclosporine A alleviated aGVHD.

Corrigendum: LYG1 Deficiency Attenuates the Severity of Acute Graft-Versus-Host Disease Skewing Allogeneic T Cells Polarization Towards Treg Cells.

[This corrects the article DOI: 10.3389/fimmu.2021.

LYG1 Deficiency Attenuates the Severity of Acute Graft-Versus-Host Disease Skewing Allogeneic T Cells Polarization Towards Treg Cells.

Acute graft-versus-host disease (aGVHD) is a lethal complication after allogeneic hematopoietic stem cell transplantation. The mechanism involves the recognition of host antigens by donor-derived T cells which induces augmented response of alloreactive T cells. In this study, we characterized the role of a previously identified novel classical secretory protein with antitumor function-LYG1 (Lysozyme G-like 1), in aGVHD.

Improved photocatalytic degradation of ketoprofen by Pt/MIL-125(Ti)/Ag with synergetic effect of Pt-MOF and MOF-Ag double interfaces: Mechanism and degradation pathway.

It is a central issue to improve the separation efficiency of photogenerated charge carriers and the utilization of visible light in the field of photocatalysis. Herein, taking MIL-125(Ti) as a host material, the Pt/MIL-125(Ti) was first prepared by solvothermal method to build the interface of Schottky junction. Ag was then introduced onto the surface of Pt/MIL-125(Ti) to form the interface with the surface plasmon resonance effect.

Establishment and characterization of a DOT1L inhibitor-sensitive human acute monocytic leukemia cell line YBT-5 with a novel KMT2A-MLLT3 fusion.

Immortalized cell lines are useful for deciphering the pathogenesis of acute leukemia and developing novel therapeutic agents against this malignancy. In this study, a new human myeloid leukemia cell line YBT-5 was established. After more than 1-year cultivation from the bone marrow of a patient with acute monocytic leukemia, YBT cell line was established.

Magnetic solid-phase extraction of pyrethroid pesticides in environmental water samples with CoFe O -embedded porous graphitic carbon nanocomposites.

Magnetic CoFe O -embedded porous graphitic carbon nanocomposites were prepared through a facile solid-phase thermal reaction with NaCl as a template. The material was applied in the magnetic solid-phase extraction process coupled with high performance liquid chromatography with a diode array detector to detect the trace fenpropathrin, cyhalothrin, S-fenvalerate, and bifenthrin in different water samples. The synthesis conditions of nanomaterial including glucose concentration and calcination time on extraction performance for pyrethroid pesticides have been investigated.

CXCR3 blockade combined with cyclosporine A alleviates acute graft-versus-host disease by inhibiting alloreactive donor T cell responses in a murine model.

Chemotaxis of T cells to acute graft-versus-host disease (aGvHD) target tissues directed by chemokines and their receptors plays a key role in the pathogenesis of aGvHD. Blockade of lymphocyte migration by targeting chemokine receptors may be a viable strategy for the prevention and treatment of aGvHD, which is quite distinguishable from typical efforts to use immunosuppressive medications that have been associated with some side effects. CXCR3 and its ligands have been reported to be correlated with aGvHD pathogenesis.

CCR5 blockade combined with cyclosporine A attenuates liver GVHD by impairing T cells function.

Objective: Our preview study found that CCR5 blockade combined with cyclosporine A could attenuate the severity of liver GVHD. But the potential immunological mechanisms have not yet been explored. So our present study was designed to clarify the potential immunological mechanisms in mouse models after allo-HSCT.

Arsenic trioxide rewires mantle cell lymphoma response to bortezomib.

Although most of the mantle cell lymphoma (MCL) patients initially responded well to bortezomib (BTZ), the dose-dependent toxicities have greatly limited the application of BTZ to MCL. To investigate the efficacy and mechanism of arsenic trioxide (ATO) with BTZ in inducing apoptosis of MCL cells, two MCL cell lines, along with primary cells from MCL patients (n = 4), were used. Additionally, the NOD-SCID mice xenograft model of Jeko-1 cells was established to study the anti-MCL mechanisms in an in vivo setting.