Figure 3.
PTPγ expression is differentially modulated by IL-4 and GM-CSF. IL-4 and GM-CSF were added, either individually or in combination, at the beginning of incubation. *IL-4 was added after 3 days of GM-CSF treatment. Some of the cells were stained with May-Grunwald; the remaining cells were analyzed by cytofluorometry with a combination of myeloid markers. Large cells with large, vacuolated cytoplasm are shown in the absence of cytokines. These cells did not express PTPγ and were characterized by a macrophage phenotype (CD14+CD64+CD1a–CD80–). PTPγ began to be expressed only when IL-4 was added, but in the absence of GM-CSF the number of cells obtained in culture was decreased and the phenotype was macrophagic. When both cytokines were added, PTPγ was expressed, and both the morphology and the surface markers shifted to those of a typical DC phenotype (CD14–CD64–CD1a+CD80+). If IL-4 addition was delayed (*), the phenotype was intermediate because CD64 was still expressed and the cytoplasmic processes typical of DCs were less apparent. ACTB expression demonstrated the specificity of the signal. Results of 1 of 3 representative experiments are shown. Shaded areas represent isotype control; open areas, the specific marker.

PTPγ expression is differentially modulated by IL-4 and GM-CSF. IL-4 and GM-CSF were added, either individually or in combination, at the beginning of incubation. *IL-4 was added after 3 days of GM-CSF treatment. Some of the cells were stained with May-Grunwald; the remaining cells were analyzed by cytofluorometry with a combination of myeloid markers. Large cells with large, vacuolated cytoplasm are shown in the absence of cytokines. These cells did not express PTPγ and were characterized by a macrophage phenotype (CD14+CD64+CD1aCD80). PTPγ began to be expressed only when IL-4 was added, but in the absence of GM-CSF the number of cells obtained in culture was decreased and the phenotype was macrophagic. When both cytokines were added, PTPγ was expressed, and both the morphology and the surface markers shifted to those of a typical DC phenotype (CD14CD64CD1a+CD80+). If IL-4 addition was delayed (*), the phenotype was intermediate because CD64 was still expressed and the cytoplasmic processes typical of DCs were less apparent. ACTB expression demonstrated the specificity of the signal. Results of 1 of 3 representative experiments are shown. Shaded areas represent isotype control; open areas, the specific marker.

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