Chemokine triggered integrin activation and actin remodeling events guiding lymphocyte migration across vascular barriers

TL;DR: An overview of the pleiotropic effects of CCL2 signaling on cells of the myeloid lineage, beyond chemotaxis, and how these actions might help to shape immune cell behavior and tumor immunity is provided.

TL;DR: The often poor prognosis of this type of lymphoma has been substantially improved by immunochemotherapy, in particular with rituximab, and despite improved outcome, a significant proportion of patients relapse, particularly those with central nervous system manifestations.

TL;DR: Current knowledge about molecular mechanisms of leukemic T- cell infiltration with special emphasis on the newly identified subtype early T-cell-progenitor (ETP)-ALL is summarized and extravasation potential of T-ALL cells is compared with that of other hematologic malignancies such as B-ALL and acute myeloid leukemia (AML).

TL;DR: The purpose of this review is to describe intestinal nutrient transportation, identify a number of widely expressed receptors and signal transduction pathways, and outline the current understanding of the mechanisms involved in health and disease.

TL;DR: 'Knockdown' of the gene encoding Mst1 demonstrated its requirement for the induction of both a polarized morphology and integrin LFA-1 clustering and adhesion triggered by chemokines and T cell receptor ligation.

TL;DR: DOCK2 and PI3Kgamma play distinct roles during T and B cell integrin activation and migration, and in vitro adhesion assays and intravital microscopy of lymphoid organ vasculature uncovered an unexpected defect inIntegrin activation in DOCK2-/- B cells, whereas lack of Dock2 did not affect chemokine-triggered integrinactivation in T cells.

TL;DR: These large multiprotein complexes assemble around the integrin family of cell adhesion molecules (transmembrane αβ heterodimers) that are typically linked with each other.

TL;DR: Inhibition experiments with blocking peptide analogues and monoclonal antibodies revealed that GRO‐α and its receptor CXCR2 but not MCP‐1 and its receptors substantially contributed to conversion of rolling into firm, shear‐resistant arrest of monocytes to TNF‐α‐stimulated endothelium in physiological flow.