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Fig. 7 | Cell Communication and Signaling

Fig. 7

From: Natural carboxyterminal truncation of human CXCL10 attenuates glycosaminoglycan binding, CXCR3A signaling and lymphocyte chemotaxis, while retaining angiostatic activity

Fig. 7

C-terminally truncated CXCL10(1–73) evokes less in vivo migration of CXCR3+ T lymphocytes upon IP injection compared to intact CXCL10(1–77). A Schematic representation of the experimental set-up. Female NMRI mice received sitagliptin via drinking water for 72 h (10 mg/day) and were intraperitoneally injected with vehicle (CO), 10 µg CXCL10(1–77) or 10 µg CXCL10(1–73) dissolved in 0.9% (w/v) NaCl 16 h prior to lavage of the peritoneal cavity. Migrated cells were analyzed through flow cytometry. Inhibition of soluble CD26 (sCD26) activity in the peritoneal lavage fluids was verified in a CD26 activity assay. B sCD26 enzymatic activity (%) in peritoneal lavage fluids of mice treated with sitagliptin and untreated mice. C Absolute numbers of T cells (gated as CD3+ NK1.1−) and D of activated CXCR3+ T cells (gated as CD3+ NK1.1− CXCR3+) were determined. Each symbol represents an individual mouse (n ≥ 6 per group). Four independent experiments were performed. Horizontal lines and error bars mark the median number of cells with interquartile range. Statistical analysis was performed using a Mann–Whitney U test (* p ≤ 0.05, *** p ≤ 0.001 for comparison to sitagliptin-treated control mice, $$ p ≤ 0.01 for comparison of CXCL10(1–73) to CXCL10(1–77))

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