Artículos de revistas
Differential expression of the fractalkine chemokine receptor (CX 3 CR1) in human monocytes during differentiation
Fecha
2015-12Registro en:
Panek, Cecilia Analía; Ramos, Maria Victoria; Mejias, María Pilar; Abrey Recalde, Maria Jimena; Fernández Brando, Romina Jimena; et al.; Differential expression of the fractalkine chemokine receptor (CX 3 CR1) in human monocytes during differentiation; Chinese Society for Immunology; Cellular & Molecular Immunology; 12; 6; 12-2015; 669-680
1672-7681
CONICET Digital
CONICET
Autor
Panek, Cecilia Analía
Ramos, Maria Victoria
Mejias, María Pilar
Abrey Recalde, Maria Jimena
Fernández Brando, Romina Jimena
Gori, María Soledad
Salamone, Gabriela Veronica
Palermo, Marina Sandra
Resumen
Circulating monocytes (Mos) may continuously repopulate macrophage (MAC) or dendritic cell (DC) populations to maintain homeostasis. MACs and DCs are specialized cells that play different and complementary immunological functions. Accordingly, they present distinct migratory properties. Specifically, whereas MACs largely remain in tissues, DCs are capable of migrating from peripheral tissues to lymphoid organs. The aim of this work was to analyze the expression of the fractalkine receptor (CX3 CR1) during the monocytic differentiation process. Freshly isolated Mos express high levels of both CX3 CR1 mRNA and protein. During the Mo differentiation process, CX3 CR1 is downregulated in both DCs and MACs. However, MACs showed significantly higher CX3 CR1 expression levels than did DC. We also observed an antagonistic CX3 CR1 regulation by interferon (IFN)-γ and interleukin (IL)-4 during MAC activation through the classical and alternative MAC pathways, respectively. IFN-γ inhibited the loss of CX3 CR1, but IL-4 induced it. Additionally, we demonstrated an association between CX3 CR1 expression and apoptosis prevention by soluble fractalkine (sCX3 CL1) in Mos, DCs and MACs. This is the first report demonstrating sequential and differential CX3 CR1 modulation during Mo differentiation. Most importantly, we demonstrated a functional link between CX3 CR1 expression and cell survival in the presence of sCX3 CL1.