Skip to main content
. 2020 Feb 11;11:111. doi: 10.3389/fimmu.2020.00111

Table 1.

Macrophage polarization in OA and cartilage regeneration.

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.