Figure 6.

The role of CCR2 in the recruitment of GR1+ monocytes. (A) Flow cytometry histograms comparing the recruitment of F4/80+CD11b+GR1+ monocytes in CCR2−/− (gray profile) or wild-type (black profile) mice after 2-h infection with 2 × 106 L. major parasites. (B) Lesion size in CCR2−/− (squares) and wild-type C57BL/6 (circles) mice after infection with 2 × 106 L. major parasites. (C) Flow cytometry profiles showing the recruitment of F4/80 intermediate, GR1+ monocytes into the peritoneum of mice after infection with 2 × 106 L. major promastigotes, before (top right) or after (bottom right) treatment with αCD41 antibody to deplete platelets. (D) The number of GR1+ monocytes in the peritoneum after infection with 2 × 106 L. major promastigotes in untreated mice (circles) or mice treated with αCD41 antibody to deplete platelets (squares). (E) The mean frequency of GR1+ monocytes recruited to footpads after L. major infection with or without prior depletion of platelets using αCD41 antibody. At least three mice per group were used in three independent experiments. (F) In vivo killing of L. major parasites. C57BL/6 mice were depleted of platelets with α-CD41 or not and CCR2−/− mice were infected with 106 metacyclic L. major promastigotes in the hind footpad. At different times, the footpads were collected and RT-PCR was performed to measure parasite levels, as described in experimental procedures. Data are representative of two independent experiments using at least three mice per group.

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