Differences in phenotypes of LNs vs BMNs and BNs during homeostasis and inflammatory stimulation. In homeostasis (left), LNs display altered expression of multiple surface receptors and their gene expression (mRNA levels) is changed. This phenotype is induced by PGE2, which acts through PKA and Tgm2. Moreover, LNs produce high levels of IL-6 that maintains their count. Activated LNs release NETs (ionomycin) and phagocytose in manner similar to BMNs and BNs but show impaired migratory activity toward various chemoattractants. In response to LPS they produce less TNF-α but more reactive oxygen species. In homeostasis their phenotype is immunosuppressive, whereas in inflammatory conditions (right), it is mixed with dominance of the anti-inflammatory response. C5a, complement component 5a; CD11b, integrin αM subunit; CD14, cluster of differentiation 14; CD62L, L-selectin; CXCR2 Ls, ligands of the C-X-C chemokine receptor type 2; CXCR4, C-X-C chemokine receptor type 4; fMLP, N‐formyl‐methionyl‐leucyl‐phenylalanine; MHCII, major histocompatibility complex II; Nr4a2, nuclear receptor 4A2; Nr4a3, nuclear receptor 4A3; Plet1, placenta-expressed transcription 1; Sca1/Ly6A, stem cell antigen-1; — unaltered levels, ↑ increased levels, ↓ decreased levels.