Abstract
Previously, we demonstrated that prostaglandin E2 (PGE2) induces C-C chemokine receptor type 7 (CCR7) expression on human monocytes, which stimulates their subsequent migration in response to the CCR7 natural ligands CCL19 and CCL21. In this study, we determined whether PGE2 affects CCR7 expression on macrophages. Flow cytometric analysis and chemotaxis assays were performed on Mono Mac-1-derived macrophage (MDMM-1) as well as unpolarized monocyte-derived macrophages (MDMs) to determine the CCR7 expression and functionality in the presence of PGE2. Data revealed that a MDMM-1 exhibited markedly downregulated CCR7 expression and functionality that were partially restored by treatment with PGE2. In MDMs, we observed a drastic downregulation of CCR7 expression and functionality that were unaffected following PGE2 treatment. Our data indicate that monocyte differentiation induces the loss of CCR7 expression and that PGE2 is unable to modulate CCR7 expression and functionality as shown previously in monocytes.
Highlights
Monocytes and macrophages orchestrate proper immune responses to pathogens
Our results demonstrate that monocyte maturation downregulates chemokine receptor type 7 (CCR7) expression in macrophages derived from Mono Mac-1 cells (MDMM-1 cells) and monocyte-derived macrophages (MDMs) from healthy donors
Our results clearly indicate that MDMM-1 cells and MDMs lose functional CCR7 expression, which inhibits their migration toward the CCR7 ligands CCL19 and CCL21
Summary
Monocytes have been demonstrated to be precursors of professional antigen-presenting cells, such as macrophages and dendritic cells (DCs) [1,2,3]. In response to danger stimuli, circulating blood monocytes migrate into damaged or infected tissues and differentiate into mature macrophages or DCs. After taking up antigens, the activated macrophages and DCs migrate to the draining lymph nodes to present the antigens to T and B cells. C-C chemokine receptor type 7 (CCR7) plays a leading role in the mechanism controlling the entry of lymphocytes and mature DCs into lymph nodes. Within lymph nodes, these cells encounter other immune cells for activation, determining the success of cellular immunity after infection [4]. Mice deficient in CCL19, CCL21, or CCR7 demonstrate defective DC trafficking and altered immune responses [6, 14, 15]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
