Cros et al. showed that CD14+CD16++ monocytes (non-classical) are segregated independently from intermediate and classical monocytes based on principal component analysis [14].
Wong et al. showed significantly different genetic profiles between intermediate and classical monocytes, which supported independent findings in humans and rhesus monkeys [13,19,22].
Intermediate monocytes produced significantly more tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) compared to the other populations; however, production of interleukins 6, 8, and 10 were approximate in intermediate and classical monocytes when compared to non-classical monocytes [14,19].
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Table 1 outlines the expression of surface markers for classical, intermediate, and non-classical monocytes.
As shown in an additional file, the distribution of the classical, intermediate and non-classical circulating subsets among CD45+ PBMCs was similar in patients and controls (see Additional file 4: Figure S1).
Population specific genetic profiles reveal a progressive increase in genes associated with maturation in intermediate and non-classical monocytes when compared with classical monocytes [19,24].
Though not dogmatic, general recognition that classical monocytes arise from the bone marrow and give rise to intermediate and non-classical monocytes has provided a platform for understanding monocyte maturation and methods of replenishment in disease states.
In particular, does the increase in CD16+ monocyte (intermediate and non-classical) frequency observed in cases of both acute and chronic inflammation result from increased differentiation or do they arise independently in response to inflammatory signaling cascades.
The authors demonstrate that the CD16+ monocytes produced TNF-α in vitro; however their gating strategy failed to distinguish intermediate and non-classical monocytes within the CD16+ population.
