A5037618026- Chemokine receptors and signaling
- interferon and immune responses
- Multiple Myeloma Research and Treatments
- Immune cells in cancer
- Immune Cell Function and Interaction
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Cancer-related gene regulation
- PI3K/AKT/mTOR signaling in cancer
- Peptidase Inhibition and Analysis
- Ferroptosis and cancer prognosis
- Cancer Research and Treatments
- Protein Degradation and Inhibitors
- Cancer-related Molecular Pathways
- Histone Deacetylase Inhibitors Research
- Eosinophilic Esophagitis
- Inhalation and Respiratory Drug Delivery
- Circular RNAs in diseases
- Safe Handling of Antineoplastic Drugs
- IL-33, ST2, and ILC Pathways
Tianjin Medical University
2023-2025
Chinese Academy of Medical Sciences & Peking Union Medical College
2024
Peking Union Medical College Hospital
2024
The University of Texas MD Anderson Cancer Center
2016
In multiple myeloma (MM), bone marrow stromal cells (BMSC) shape a unique niche within the marrow, promoting T-cell dysfunction and driving MM progression; however, precise underlying mechanisms remain elusive. Here, we show that BMSC-mediated reprogramming of led to heightened production CXCL10. CXCL10 orchestrated recruitment γδ T into this was observed in both Vk*MYC 5TGM1 mouse models MM, as well patients experiencing refractory or relapsed MM. Furthermore, dysfunctional exhibited...
Idiopathic pulmonary fibrosis (IPF) is a heterogeneous group of lung diseases with different etiologies and characterized by progressive fibrosis. This disease usually causes structural remodeling decreased function. The median survival IPF patients 2–5 years. Predominantly accumulation type II innate immune cells accelerates progression secreting multiple pro-fibrotic cytokines. Group 2 lymphoid (ILC2) monocytes/macrophages play key roles in immunity aggravate the formation environment. As...
<div>Abstract<p>In multiple myeloma (MM), bone marrow stromal cells (BMSC) shape a unique niche within the marrow, promoting T-cell dysfunction and driving MM progression; however, precise underlying mechanisms remain elusive. Here, we show that BMSC-mediated reprogramming of led to heightened production CXCL10. CXCL10 orchestrated recruitment γδ T into this was observed in both Vk*MYC 5TGM1 mouse models MM, as well patients experiencing refractory or relapsed MM. Furthermore,...
<p>supplementary figures and legends</p>
<p>supplementary figures and legends</p>
<div>Abstract<p>In multiple myeloma (MM), bone marrow stromal cells (BMSC) shape a unique niche within the marrow, promoting T-cell dysfunction and driving MM progression; however, precise underlying mechanisms remain elusive. Here, we show that BMSC-mediated reprogramming of led to heightened production CXCL10. CXCL10 orchestrated recruitment γδ T into this was observed in both Vk*MYC 5TGM1 mouse models MM, as well patients experiencing refractory or relapsed MM. Furthermore,...