Fig. 4: IL-34 deletion increases intra-synovial NETs in K/BxN serum transfer arthritis. | Laboratory Investigation

Fig. 4: IL-34 deletion increases intra-synovial NETs in K/BxN serum transfer arthritis.

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

Fig. 4

A Experimental scheme. Synovial tissue was analyzed for neutrophils expressing, a key early NETosis marker (citrullinated histone H3 [Cit H3]), after inducing arthritis in IL-34 KO and WT mice using flow cytometry. B Number and frequency of neutrophils expressing Cit H3 in IL-34 KO and WT detected by flow cytometry (n = 4/group). Representative of two similar experiments. C After inducing arthritis, we injected (iv) MacGreen BM (EGFP+) cells into IL-34 KO and WT mice (day 7). After sacrificing (day 10) synovial tissue was analyzed for infiltrating EGFP+ cells expressing Cit H3 by flow cytometry (Scheme). Number and frequency of total EGFP+ cells (D), EGFP+ neutrophils (E), EGFP+ NETs (identified by the expression of Cit H3) (F), and EGFP+ Mø (G); using relevant markers by flow cytometry (n = 5–6/group). H, I Intra-synovial chemokine transcripts were analyzed using qPCR in IL-34 KO and WT mice after inducing arthritis (d8, n = 4-6/group). Chemokine expression is displayed for chemokines that recruit neutrophils (H), and chemokines that recruit Mø (I). Data are represented as the means ± SEM. #P < 0.08. +P < 0.06. *P < 0.05. **P < 0.01; two-tailed, Mann–Whitney U test.

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