Fig. 6: IL-34 and PTPRZ-mediated mechanisms skew Mø towards a reparative “M2” phenotype in the synovium during K/BxN serum-transfer arthritis. | Laboratory Investigation

Fig. 6: IL-34 and PTPRZ-mediated mechanisms skew Mø towards a reparative “M2” phenotype in the synovium during K/BxN serum-transfer arthritis.

From: IL-34 and protein-tyrosine phosphatase receptor type-zeta-dependent mechanisms limit arthritis in mice

Fig. 6

A Experimental scheme for the analysis of destroyer “M1” and reparative “M2” markers in IL-34, PTPRZ KO and WT in synovial tissue by flow cytometry. B–D Reparative “M2” Mø markers in synovial tissue of IL-34, PTPRZ KO and WT mice after induction of arthritis (day 10). Representative of two similar experiments. B Number and frequency of CD163+ Mø. C Number and frequency of CD301+ Mø myeloid cells. D Number and frequency of CX3CR1+MHC-II- Mø. E Inflammatory destroyer “M1” Mø detected by the high expression of Ly6C in synovial tissue of IL-34, PTPRZ KO and WT mice after induction of arthritis (day 10). Representative of two similar experiments. F Mean Fluorescent Intensity (MFI) of relevant cytokine Mø destroyer “M1” markers, (iNOS, TNF-α) and IL-10 in synovial Mø of IL-34, PTPRZ KO and WT mice. Data are represented as the means ± SEM (n = 4–5/group). +P < 0.07. *P < 0.05. **P < 0.01; two-tailed, Mann–Whitney U test.

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