Blood monocyte subpopulations have been defined in humans initially, and the two major types of monocytes are the CD14++ CD16− and the CD14+ CD16+ monocytes. These cells have been shown to exhibit distinct phenotype and function, and the CD14+ CD16+ were labeled "proinflammatory" based on higher expression of proinflammatory cytokines and higher potency in antigen presentation. However, some pathogens like Mycobacterium tuberculosis, are known to skew CD14+ CD16+ to favor their fitness (they display lower ability to differentiate into DC-SIGN(low) CD86 (low) dendritic cells with a lower capacity to present antigen), involving p38 kinase signalling. Here, I wonder whether CD16 could play additional roles other than serving as a biological marker.
Triggering via CD16 enhances expression of some proinflammatory genes. However, it will also increase expression of anti-inflammatory genes like IL1Ra. See Shalova et al J Immunol. 2012 Apr 15;188(8):3584-93.
Please note that the Shalova study has used anti-CD16 monoclonal antibody not just immune complexes. This makes this report very convincing.
When activating monocytes then induction of pro-inflammatory mediators often is followed by induction of anti-inflammatory mediators. However, an informative feature of the CD16 receptor is that its cytoplasmic part contains an ITAM domain, such that activating pathways are favoured.
Dear Loems Ziegler-Heitbrock and Seppe Vander Beken,
I would like to thank you both for the information provided. This question forum has been very helpful so far.
Cheers,
Geanncarlo