Table 1.
Macrophage polarization | Stimuli | Transcription factors | Phenotype | Released products | Functional roles | Potential tools for OA treatment |
---|---|---|---|---|---|---|
M1 | IFN-g, LPS, TNF-a | IRF1, IRF5, IRF8, Pu.1, STAT1, STAT2, NFkB | CD80, CD86, CD40, MHC-II | TNF-a, IL-1b, IL-6, IL-12, IL-23, OSM, NO, CXCL10, IL-8, CCL5, CXCL9, CXCL11, MMP1, MMP3, MMP9, MMP13, ADAMTS | Inflammation, type 1 response and tissue injury microbicidal. → OA induction. |
M1 blocker** Depletion of CD14+ Macrophages** |
M2 | IL-4, IL-13, IL-10 and TLRs agonists, MSCs (?) | IRF4, Pu.1, SOCS1, STAT6, JMJD3, PPARg, PPARd, GATA3, C/EBPb | ARG-1, CD163, CD206 | IL-10, IL-1RA, TGF-b, IGF, CCL18, CCL4, CCL13, CCL17, MMP1, MMP12 | Anti-inflammatory response, type 2 response, tissue repair, chondrogeneic and turnover of extracellular matrix. → Cartilage regeneration. |
M2 inducers: oxLDL, collagen type II, MSCs*. Blocking mTOR pathway?** |
The M2 polarization can be halt by the microenvironment.
Further studies are required.
OA, osteoarthritis.
Bold is used to highlight information.