When stimulated through CD137 ligand murine monocytes responded just as human monocytes with an increased adherence, morphological changes, proliferation and an increase in viable cell numbers.
After activation with GM-CSF, murine monocytes were found to overexpress some surface markers of specialized macrophages and some stimulatory molecules while showing decreased expression of a marker for alternatively activated monocytes.
Stroma depleted nonadherent, M-CSF dependent bone marrow monocytes (BMM) and RAW264.7 murine monocytes (ATCC, UK) were incubated in MEM and Earle's salts (EMEM) supplemented with 10% FCS (Autogen Bioclear, UK), 2 mmol/l glutamine, 100 IU/ml benzylpenicillin, and 100 mg/ml streptomycin (all from Sigma, UK).
CCR2, for example, is preferentially expressed on Ly6Chigh murine monocytes and has provided evidence for their functional similarity to classical human monocytes.
Using gene array technology, we could establish that glucocorticoids, that are among the most widely used anti-inflammatory drugs, would reprogram monocytes to confer anti-inflammatory functions in human and murine monocytes [11 13].
Presently, murine monocytes are evenly distributed by their relative expression of the Ly6C antigen and are, for the most part, functionally distinct [34-39] [34-39]
While human monocytes differentiate to inflammatory DCs murine monocytes do not.
It induces activation of human and murine monocytes and macrophages, monocyte migration, survival and even proliferation.
Based on the reports with human CD137L-DCs we expected CD137 ligand signaling to induce differentiation of murine monocytes to inflammatory DCs.
This is in line with the missing IL-12 secretion, expression of costimulatory molecules and the T cell stimulatory activity of CD137-Fc-treated murine monocytes.
