Figure 3
Figure 3. Deletion of Cdc42 results in decreased production of antigen-specific antibodies. (A) Splenocytes from WT and Cdc42−/− (KO) mice were immunolabeled with antibodies against CD93, CD38, and CD138, and analyzed by flow cytometry for CD93−CD38+CD138+ plasma cells. (B) Serum from WT and KO mice was subjected to ELISA analysis for IgM, IgG, and IgA. (C-F) Mice were injected intraperitoneally with 100 μg NP-KLH precipitated with alum (E-F), or with 10 μg TNP-Ficoll (C-D). Serum was collected at different time points. Microtiter plates were coated with either 20 μg/mL NP-BSA for capturing NP-specific IgM and IgG1 in serum of NP-KLH–treated mice (E-F), or with 20 μg/mL TNP-BSA for capturing TNP-specific IgM and IgG3 in serum of TNP-Ficoll–treated mice (C-D). Bound antigen-specific antibodies were detected using specific HRP-conjugated goat anti–mouse antibodies (**P < .01; *P < .05). Data represent means ± SD.

Deletion of Cdc42 results in decreased production of antigen-specific antibodies. (A) Splenocytes from WT and Cdc42−/− (KO) mice were immunolabeled with antibodies against CD93, CD38, and CD138, and analyzed by flow cytometry for CD93CD38+CD138+ plasma cells. (B) Serum from WT and KO mice was subjected to ELISA analysis for IgM, IgG, and IgA. (C-F) Mice were injected intraperitoneally with 100 μg NP-KLH precipitated with alum (E-F), or with 10 μg TNP-Ficoll (C-D). Serum was collected at different time points. Microtiter plates were coated with either 20 μg/mL NP-BSA for capturing NP-specific IgM and IgG1 in serum of NP-KLH–treated mice (E-F), or with 20 μg/mL TNP-BSA for capturing TNP-specific IgM and IgG3 in serum of TNP-Ficoll–treated mice (C-D). Bound antigen-specific antibodies were detected using specific HRP-conjugated goat anti–mouse antibodies (**P < .01; *P < .05). Data represent means ± SD.

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