Decoy Receptors in Autoimmunity: Molecular Guardians and Pathogenic Players in Immune Dysregulation. [PDF]
Autoimmune disorders encompass a varied range of diseases in which the immune system mistakenly targets and attacks the body’s own tissues. The causes of the conditions are unknown. It is presumed that various genetic, environmental, and immune factors all play a part.
Farahani H +4 more
europepmc +2 more sources
Phosphoproteomic mapping of CCR5 and ACKR2 signaling properties. [PDF]
ACKR2 is an atypical chemokine receptor which is structurally uncoupled from G proteins and is unable to activate signaling pathways used by conventional chemokine receptors to promote cell migration.
Vacchini A +11 more
europepmc +3 more sources
Bystander Expression of Atypical Chemokine Receptor 2 Protects T Cells from Chemoattraction towards Cancer-Associated Fibroblasts. [PDF]
Cancer‐associated fibroblasts (CAFs) secrete chemokines that attract T cells. Here we show that the overexpression of atypical chemokine receptor 2 (ACKR2) by bystander cells scavenges key chemokines secreted by CAFs, including previously unreported ligands CXCL12 and CXCL1, and thereby protects T cells from chemoattraction by CAFs.
Tang R +7 more
europepmc +2 more sources
Single-Cell Profiling Reveals Conserved Differentiation and Partial EMT Programs Orchestrating Ecosystem-Level Antagonisms in Head and Neck Cancer. [PDF]
ABSTRACT Head and neck squamous cell carcinoma (HNSC) exhibits profound intratumoral heterogeneity, driven by dynamic interactions between malignant cells and the tumour microenvironment (TME). Using consensus non‐negative matrix factorisation (cNMF) on multi‐site HNSC single‐cell transcriptomes, we resolving conserved meta‐programs define cellular ...
Jiang D +7 more
europepmc +2 more sources
Chemokines: Orchestration of the Tumor Microenvironment and Control of Hepatocellular Carcinoma Progression. [PDF]
ABSTRACT Chemokines, a family of chemotactic cytokines, play a central role in shaping the tumor microenvironment (TME) and in influencing the progression of hepatocellular carcinoma (HCC), a well‐known inflammation‐related cancer. This review addresses the intricate interplay between chemokines and HCC and highlights their multifaceted role.
Yang J, Lu H, Li L.
europepmc +2 more sources
Eosinophils promote monocyte to macrophage differentiation and anti-bacterial immunity [PDF]
Chemokine receptors control cell migration within the body. Here we reveal a novel interaction between eosinophils and monocytes in the bone marrow, indirectly controlled by the atypical chemokine receptor ACKR2.
Wilson GJ +10 more
europepmc +2 more sources
The atypical chemokine receptor ACKR2 is protective against sepsis [PDF]
Sepsis is a systemic inflammatory response as a result of uncontrolled infections. Neutrophils are the first cells to reach the primary sites of infection and chemokines play a key role in recruiting neutrophils.
Alves-Filho, José Carlos +15 more
core +1 more source
The atypical chemokine receptor Ackr2 constrains NK cell migratory activity and promotes metastasis [PDF]
Chemokines have been shown to be essential players in a range of cancer contexts. In this study, we demonstrate that mice deficient in the atypical chemokine receptor Ackr2 display impaired development of metastasis in vivo in both cell line and ...
Brownlie, Demi +12 more
core +1 more source
CCRL2 Expression by Specialized Lung Capillary Endothelial Cells Controls NK-cell Homing in Lung Cancer [PDF]
Patterns of receptors for chemotactic factors regulate the homing of leukocytes to tissues. Here we report that the CCRL2/chemerin/CMKLR1 axis represents a selective pathway for the homing of natural killer (NK) cells to the lung.
Bernardini G. +20 more
core +1 more source
Elevated ACKR2 expression is a common feature of inflammatory arthropathies [PDF]
Objectives. Chemokines are essential contributors to leucocyte accumulation at sites of inflammatory pathology. Interfering with chemokine or chemokine receptor function therefore represents a plausible therapeutic option.
Baldwin, Helen M. +6 more
core +1 more source

