Granulocyte-macrophage colony-stimulating factor and other cytokines regulate surface expression of the leukocyte adhesion molecule-1 on human neutrophils, monocytes, and their precursors.

• DOI: 10.4049/jimmunol.145.2.576
• Publication Date: 2022-12-31T06:26:02Z
• Authors: J D Griffin; O Spertini; T J Ernst; M P Belvin; H B Levine; Y Kanakura; T F Tedder
• Keywords: Monocyte

Abstract There is increasing evidence that cytokines such as granulocyte-macrophage (GM)-CSF can profoundly affect the adhesion, aggregation, and mobility of neutrophils both in vitro vivo. However, mechanisms whereby these factors might alter adhesive properties are incompletely understood. A new family cellular adhesion molecules has recently been identified by cDNA cloning. The members this include human leukocyte molecule-1 (LAM-1), endothelial-leukocyte molecule, mouse homing receptor for high endothelial venules, MEL-14. LAM-1 homologue murine MEL-14, believed to mediate binding leukocytes venules. be mAb TQ-1, Leu 8, or anti-LAM1.1. expression regulation on granulocytes, monocytes, their precursors was investigated using flow cytometry anti-LAM-1.1 mAb. Neutrophils, eosinophils, marrow myeloid cells, granulocyte/macrophage colony-forming unit, burst-forming unit erythroid cells were LAM-1+ microfluorimetry. tested treating various cell populations with other stimuli 0-90 min. Exposure neutrophils, GM-CSF induced rapid complete loss from surface, but had no effect lymphocytes. temporally correlated up-regulation CD11b (Mo1), an molecule involved neutrophil aggregation. Several known activate also caused down-regulation CD11b, including TNF, FMLP, leukotriene B4. Interestingly, granulocyte-CSF IFN-gamma minimal effects expression. Similar results observed monocytes precursor cells. Thus, exposure a profound change surface molecules, coordinated LAM-1. These changes proteins likely aggregation mature patients receiving certain types cytokine therapy.