Figure 4.
BCL-XL inhibitor preferentially targets neutrophils at sites of inflammation, without systemic depletion of other immune cell populations in mice, apart from platelets. STIA was induced in B6 mice by IP injection of K/BxN serum. Arthritic mice were treated for 5 days with 100 mg/kg BCL-XL inhibitor or vehicle by oral gavage starting d2 postserum injection. Following inhibitor treatment (d7 postserum injection) viable neutrophils (PMN), monocyte/macrophage (mono/mac; M), T cells (T), B cells (B), plasmacytoid dendritic cell (pDC; P), conventional dendritic cell (cDC; C) were enumerated in (A-B) blood and (D-E) spleen by PI staining and flow cytometry. Platelets were enumerated in whole blood by analysis on an Advia 2120i automated hematological analyzer (C). Data shown were pooled from 2 experiments (n = 10 mice/group; mean ± SEM). All data analyzed using a 2-tailed Student t test. *P < .05, **P < .01, ***P < .001.

BCL-XL inhibitor preferentially targets neutrophils at sites of inflammation, without systemic depletion of other immune cell populations in mice, apart from platelets. STIA was induced in B6 mice by IP injection of K/BxN serum. Arthritic mice were treated for 5 days with 100 mg/kg BCL-XL inhibitor or vehicle by oral gavage starting d2 postserum injection. Following inhibitor treatment (d7 postserum injection) viable neutrophils (PMN), monocyte/macrophage (mono/mac; M), T cells (T), B cells (B), plasmacytoid dendritic cell (pDC; P), conventional dendritic cell (cDC; C) were enumerated in (A-B) blood and (D-E) spleen by PI staining and flow cytometry. Platelets were enumerated in whole blood by analysis on an Advia 2120i automated hematological analyzer (C). Data shown were pooled from 2 experiments (n = 10 mice/group; mean ± SEM). All data analyzed using a 2-tailed Student t test. *P < .05, **P < .01, ***P < .001.

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