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. 2022 Jun 15;8(24):eabo4271. doi: 10.1126/sciadv.abo4271

Fig. 5. CD38 inhibition reverses mitochondrial defect and restores CD8+ T cell function in BXD2 lupus mice against LCMV infection.

Fig. 5.

(A and B) Percentage of positive cells expressing CD107a (A) and granzyme B (B) in gp33+ CD8+ T cells 8 days after LCMV Armstrong infection from diseased BXD2 treated with control water or MK-0159. (C) Percentage of depolarized mitochondria in gp33+ CD8+ T cells 8 days after LCMV Armstrong infection from diseased BXD2 treated with control water or MK-0159. (D) LCMV viral load 8 days after LCMV Armstrong infection using qPCR of glycoprotein gene normalized by tissue ACTB in diseased BXD2 treated with control water or MK-0159. (E to G) Representative liver histology 8 days after LCMV Armstrong infection from diseased BXD2 treated with control water (E) or MK-0159 (F) and their respective hepatitis activity index (G). (H and I) Percentage of positive cells expressing CD107a (H) and granzyme B (I) in gp33+ CD8+ T cells 8 days after LCMV Armstrong infection from diseased BXD2 treated with control NP or NP-MK-0159. (J to M) Representative liver histology 8 days after LCMV Armstrong infection from diseased BXD2 treated with NP-control with the presentation of necrosis (J) or portal and periportal inflammation (K) or treated with NP-MK-0159 (L) and their respective hepatitis activity index (M). (N) LCMV viral load 8 days after LCMV Armstrong infection using qPCR of glycoprotein gene normalized by tissue ACTB in diseased BXD2 treated with NP-control or NP-MK-0159. (O) Percentage of depolarized mitochondria in gp33+ CD8+ T cells 8 days after LCMV Armstrong infection from diseased BXD2 treated with NP-control or NP-MK-0159. (P and Q) MFI of PINK1 (P) and LysoSensor Green (Q) in gp33+ CD8+ T cells 8 days after LCMV Armstrong infection from diseased BXD2 treated with NP-control or NP-MK-0159. Data are means ± SD; statistical analysis by two-tailed t test. *P < 0.05, **P < 0.01.