Figure 1
Establishment of murine models of steroid therapy in ITP. (A) The passive model of ITP was generated by injecting anti-β3 integrin polysera or mAbs (9D2, PSI C1, or JAN C1) into WT BALB/c mice. Administration of DEX (10 mg/kg intraperitoneally) 4 hours after mAb injection and continuing daily increased platelet number significantly compared with PBS-treated mice. Mean ± SD. N = 9. (B-C) The active model of ITP was generated in WT mice via engraftment of immunized β3−/− splenocytes (B, 2.5×106; C, 1×106). Administration of DEX (B) orally (N = 22, beginning on day 6) or (C) intraperitoneally (N = 13, beginning at day 6) significantly increased platelet count. *P < .05, **P < .01, ***P < .001 vs water control or PBS. Mean ± SD.

Establishment of murine models of steroid therapy in ITP. (A) The passive model of ITP was generated by injecting anti-β3 integrin polysera or mAbs (9D2, PSI C1, or JAN C1) into WT BALB/c mice. Administration of DEX (10 mg/kg intraperitoneally) 4 hours after mAb injection and continuing daily increased platelet number significantly compared with PBS-treated mice. Mean ± SD. N = 9. (B-C) The active model of ITP was generated in WT mice via engraftment of immunized β3−/− splenocytes (B, 2.5×106; C, 1×106). Administration of DEX (B) orally (N = 22, beginning on day 6) or (C) intraperitoneally (N = 13, beginning at day 6) significantly increased platelet count. *P < .05, **P < .01, ***P < .001 vs water control or PBS. Mean ± SD.

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