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Fig. 4 | Arthritis Research & Therapy

Fig. 4

From: The caspase-8/RIPK3 signaling axis in antigen presenting cells controls the inflammatory arthritic response

Fig. 4

The caspase-8-receptor-interacting serine-threonine kinase 3 (RIPK3) signaling axis functions in the naive joint independent of cell death. B6.CD45.1 mice reconstituted with equal portions of B6.CD45.1/2 (wild-type (WT)) and either Casp8 flox/flox (control, n = 5), Cre CD11c Casp8 flox/flox (n = 4) or RIPK3 –/– Cre CD11c Casp8 flox/flox (n = 4) fluorescence-activated cell sorting (FACS)-sorted Lin-Sca-1+c-kit + (LSK) populations were maintained on low-dose oral antibiotics. Data are representative of two individual studies. a Representation of chimera generation. Chimeric mice were evaluated 8 weeks post-transfer for distribution of WT (45.1/2) and control, Cre CD11c Casp8 flox/flox or RIPK3 –/– Cre CD11c Casp8 flox/flox (45.2)-derived synovial populations of Ly6ChiCD64lo cells (b), Ly6CintCD64- cells (c), Ly6CloCD64- cells (d), CD11b+ dendritic cells (e), neutrophils (f), eosinophils (g), MHC II+ macrophages (h) and MHC II macrophages (i). Error bars for 45.1/2-derived and 45.2-derived synovial populations are directed down; error bars for recipient-derived synovial populations are directed up. PMN polymorphonuclear cells

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