Antitumor response of CD14+/CD16+ monocyte subpopulation

Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16+ monocyte population via the IL-10/STAT3 axis

“…Expanding upon our previous observation that the monocyte compartment becomes perturbed in TB patients [18], we now report that the CD163 + MerTK + pSTAT3 + signature accompanies the expansion of the CD16 + monocytes. As these results contrast with the pro-inflammatory phenotype of CD16 + monocytes in healthy donors [13,[15][16][17], we infer that all CD16 + monocytes are not created in a similar manner, and thus the CD16 expression in monocyte-macrophages cannot be extrapolated to indicate a pro-or anti-inflammatory nature. Their final differentiation program might result as a consequence of the microenvironment shaped in health and disease pro-npg www.cell-research.com | Cell Research gression contexts.…”

“…Notably, the CD16 + subset accounts for only 10% of the total monocyte population in healthy donors, displaying a unique cell-surface marker expression and cytokine secretion pattern in comparison with its CD16 − counterpart [13,14]. Indeed, upon stimulation with lipopolysaccharide, CD16 + monocytes isolated from healthy donors secrete higher amounts of pro-inflammatory factors such as tumor necrosis factor-alpha (TNFα), interleukin-1-beta (IL-1) and IL-6, but low amount of the anti-inflammatory mediator IL-10 [13,[15][16][17]. Other features distinguishing the CD16 + subset are higher antigen processing and presentation, pro-angiogenic behavior and motility [10].…”

Effects of an exercise challenge on mobilization and surface marker expression of monocyte subsets in individuals with normal vs. elevated blood pressure

“…These cells are shown to exhibit dendritic cell (DC)-like characteristics indicated by surface markers (Ancuta et al, 2000;Grage-Griebenow et al, 2001), to become DCs when cultured and stimulated in vitro, to express higher levels of CD1a, CD11a, and CD11c (Sanchez-Torres et al, 2001), to be more mature, to be more potent antigen presenting cells, to produce less cytokines, and to show less phagocytic activity compared to CD16 − monocytes (CD16 − CD14 + ) (Ziegler-Heitbrock, 1996). However, the findings are mixed on their maturity and cytokine production (Clanchy et al, 2006;Szaflarska et al, 2004). CD16 + CD14 + monocytes are also shown to express less CCR2 (MCP-1 receptor) but higher levels of CCR5 (receptor for various chemokines including macrophage inflammatory protein-1 alpha; MIP-1α, MIP-1β, RANTES) than CD16 − CD14 + monocytes, suggesting that CD16 + monocytes may exhibit different trafficking patterns from CD16 − monocytes (Weber et al, 2000).…”

Clinical immunology Gastric cancer increase the percentage of intermediate (CD14++CD16+) and nonclassical (CD14+CD16+) monocytes

“…Strong anti-inflammatory signal in association with the action of chemotactic factors is reflected by monocyte differentiation to MII macrophages, as a result promoting the growth of neoplastic tissue. Monocytes with CD14+CD16+ phenotype show the highest anti-neoplastic activity in vitro, among others exerting cytotoxic and cytostatic effects on malignant cells, as well as synthesizing and secreting high amounts of pro-inflammatory cytokines (TNF-α, IL-12p40/p70) [26]. The observed increase in the fraction of monocytes from this subpopulation, in peripheral blood of patients, is undoubtedly associated with the immune system response against malignant cells circulating in the peripheral blood.…”