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Modulation of Lymphotoxin β Surface Expression by Kaposi's Sarcoma-Associated Herpesvirus K3 Through Glycosylation Interference.
J Med Virol
January 2025
Department of Infection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) employs diverse mechanisms to subvert host immune responses, contributing to its infection and pathogenicity. As an immune evasion strategy, KSHV encodes the Membrane-Associated RING-CH (MARCH)-family E3 ligases, K3, and K5, which target and remove several immune regulators from the cell surface. In this study, we investigate the impact of K3 and K5 on lymphotoxin receptor (LTβR) ligands, LTβ and LIGHT, which are type II transmembrane proteins and function as pivotal immune mediators during virus infection.
View Article and Find Full Text PDFIL-33-activated ILC2s induce tertiary lymphoid structures in pancreatic cancer.
Nature
January 2025
Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Tertiary lymphoid structures (TLSs) are de novo ectopic lymphoid aggregates that regulate immunity in chronically inflamed tissues, including tumours. Although TLSs form due to inflammation-triggered activation of the lymphotoxin (LT)-LTβ receptor (LTβR) pathway, the inflammatory signals and cells that induce TLSs remain incompletely identified. Here we show that interleukin-33 (IL-33), the alarmin released by inflamed tissues, induces TLSs.
View Article and Find Full Text PDFDeletion of lymphotoxin-β receptor (LTβR) protects against acute kidney injury by PPARα pathway.
Mol Med
December 2024
Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1095 Jiefang Road, Wuhan, 430030, China.
Article Synopsis
- Recent findings reveal that the lymphotoxin-β receptor (LTβR) plays a significant role in inflammation, but its exact functions in acute kidney injury (AKI) are still not well understood.
- In mouse models of AKI induced by renal ischemia-reperfusion, depletion of LTβR led to reduced kidney damage and inflammation, suggesting that LTβR primarily affects renal parenchymal cells during injury.
- RNA sequencing showed that the protective effects observed with LTβR depletion are linked to the activation of PPARα signaling, indicating that targeting the LTβR/PPARα pathway could offer new therapeutic strategies for managing AKI.
NF-κB associated markers of prognosis in early and metastatic triple negative breast cancer.
Breast Cancer Res
December 2024
Department of Obstetrics and Gynecology, Program in Women's Oncology, Women and Infants Hospital, Providence, Rhode Island, USA.
Background: Triple negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. While PD-1 based immunotherapies overall have led to improved treatment outcomes for this disease, a diverse response to frontline chemotherapy and immunotherapy still exist in TNBC, highlighting the need for more robust prognostic markers.
Methods: Tumor-intrinsic immunotranscriptomics, serum cytokine profiling, and tumor burden studies were conducted in two syngeneic mouse models to assess differential effects in both the early-stage and metastatic setting.
Regulatory T cells crosstalk with tumor cells and endothelium through lymphotoxin signaling.
Nat Commun
December 2024
Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Regulatory T cells (Tregs) with multifaceted functions suppress anti-tumor immunity by signaling surrounding cells. Here we report Tregs use the surface lymphotoxin (LT)α1β2 to preferentially stimulate LT beta receptor (LTβR) nonclassical NFκB signaling on both tumor cells and lymphatic endothelial cells (LECs) to accelerate tumor growth and metastasis. Selectively targeting LTβR nonclassical NFκB pathway inhibits tumor growth and migration in vitro.
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