CD1c+ blood dendritic cells have Langerhans cell potential.
Newcastle upon Tyne, United Kingdom. In Blood, 28 Nov 2014
Here we show that, while monocytes are able to express langerin, when cultured with soluble ligands GM-CSF, TGFβ and BMP7, CD1c(+) dendritic cells become much more LC-like with high langerin, Birbeck granules, EpCAM and Ecadherin expression, under the same conditions.
The atypical chemokine receptor ACKR2 suppresses Th17 responses to protein autoantigens.
Glasgow, United Kingdom. In Immunol Cell Biol, 28 Nov 2014
Interestingly, after immunization with protein, but not peptide, antigen, Ackr2 deficiency was also associated with an increase in lymph node B cells expressing granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that enhances T helper type 17 (Th17) cell development and survival.
Pulmonary macrophage transplantation therapy.
Cincinnati, United States. In Nature, 23 Nov 2014
Here, using granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor-β-deficient (Csf2rb(-/-)) mice that develop a myeloid cell disorder identical to hereditary pulmonary alveolar proteinosis (hPAP) in children with CSF2RA or CSF2RB mutations, we show that pulmonary macrophage transplantation (PMT) of either wild-type or Csf2rb-gene-corrected macrophages without myeloablation was safe and well-tolerated and that one administration corrected the lung disease, secondary systemic manifestations and normalized disease-related biomarkers, and prevented disease-specific mortality.
High-dimensional analysis of the murine myeloid cell system.
Singapore, Singapore. In Nat Immunol, 12 Nov 2014
Using mice that cannot sense granulocyte macrophage-colony stimulating factor GM-CSF (Csf2rb(-/-)), which have discrete alterations in myeloid development, we confirmed differences in barrier tissue dendritic cells, lung macrophages and eosinophils.
Secondary pulmonary alveolar proteinosis in hematologic malignancies.
Weston, United States. In Hematol Oncol Stem Cell Ther, 06 Nov 2014
Idiopathic PAP occurs as a result of auto-antibodies directed against granulocyte-macrophage colony stimulating factor (GM-CSF) impeding the surfactant clearing function of alveolar macrophages leading to progressive respiratory failure.
Targeting Th17 cells in autoimmune diseases.
Cambridge, United States. In Trends Pharmacol Sci, 14 Sep 2014
Given that Th17 cells express IL-17 together with many other proinflammatory cytokines [IL-17F, IL-22, IL-26, and granulocyte-macrophage colony-stimulating factor (GM-CSF)], targeting the Th17 cell lineage may be superior to blocking a single effector cytokine.