Expression of CCR6 and CD83 by cytokine-activated human neutrophils

Blood. 2000 Dec 1;96(12):3958-63.

Abstract

Polymorphonuclear leukocytes (PMNLs) are thought to be terminally differentiated, short-lived, and unable to actively synthesize new proteins or to interact with T cells. In the current study, it was found that PMNLs incubated with supernatants of phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PHA-sup) expressed high levels of CCR6 mRNA. Neutralization with IgG against several cytokines revealed that tumor necrosis factor (TNF)-alpha was largely responsible for the PHA-sup-induced CCR6 mRNA expression. Among recombinant cytokines, TNF-alpha induced high levels of CCR6 mRNA expression, whereas interferon (IFN)-gamma induced low levels. The 2 cytokines together exhibited a considerable synergy. Cytokine-activated PMNLs expressed functional CCR6, as detected by the binding of sodium iodide I 125-labeled liver and activation-regulated chemokine (LARC) and dose-dependent migration toward LARC. The induction of CCR6 suggested that these cytokine-activated PMNLs have more similarities with dendritic cells (DCs) that express CCR6 in an immature stage. In fact, the activation of PMNLs with TNF-alpha and IFN-gamma induced the expression of CD83, a dominant cell-surface marker of DCs. When PMNLs were activated with granulocyte macrophage-colony-stimulating factor, TNF-alpha, and IFN-gamma, these cells expressed CD40 and HLA-DR in addition to CD83. Taken together, PMNLs, under appropriate conditions, can undergo a differentiation process characterized by the acquisition of new phenotypes and functions, and such differentiated PMNLs may play more active roles in the adaptive immune response. (Blood. 2000;96:3958-3963)

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD
  • CD83 Antigen
  • Cell Differentiation / drug effects
  • Chemokine CCL20
  • Chemokines, CC / metabolism
  • Chemotaxis, Leukocyte / drug effects
  • Cytokines / pharmacology*
  • Gene Expression / drug effects
  • Humans
  • Immunoglobulins / biosynthesis
  • Immunoglobulins / drug effects*
  • Immunoglobulins / genetics*
  • Immunophenotyping
  • Interferon-gamma / pharmacology
  • Macrophage Inflammatory Proteins*
  • Membrane Glycoproteins / biosynthesis
  • Membrane Glycoproteins / drug effects*
  • Membrane Glycoproteins / genetics*
  • Neutrophil Activation / drug effects
  • Neutrophil Activation / genetics
  • Neutrophil Activation / immunology
  • Neutrophils / cytology
  • Neutrophils / drug effects*
  • Neutrophils / immunology
  • RNA, Messenger / drug effects
  • RNA, Messenger / metabolism
  • Receptors, CCR6
  • Receptors, CCR7
  • Receptors, Chemokine / biosynthesis
  • Receptors, Chemokine / drug effects*
  • Receptors, Chemokine / genetics*
  • Tumor Necrosis Factor-alpha / pharmacology
  • Up-Regulation / drug effects

Substances

  • Antigens, CD
  • CCL20 protein, human
  • CCR6 protein, human
  • CCR7 protein, human
  • Chemokine CCL20
  • Chemokines, CC
  • Cytokines
  • Immunoglobulins
  • Macrophage Inflammatory Proteins
  • Membrane Glycoproteins
  • RNA, Messenger
  • Receptors, CCR6
  • Receptors, CCR7
  • Receptors, Chemokine
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma