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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Nat Immunol. 2009 Mar 8;10(4):412–419. doi: 10.1038/ni.1712

Figure 4.

Figure 4

Defective plasma cell formation in Slc3a2f/fCD19-Cre+ mice. (a,b) In vitro plasma cell formation. Resting splenic B cells (CD43−CD98hc-deficient) were purified from Slc3a2f/fCD19-Cre+ or littermate control mice, cultured with LPS for 5 days, and stained for surface IgG3 (a) and CD138 (b) (Syndecan-1, a plasma cell marker). Cells were analyzed by flow cytometry. Dot plot is representative data from one mouse; bar graphs summarize IgG3 or CD138 staining on B220lo cells. Error bars show s.e.m. from 3 mice per group. **P < 0.025 Experiment was repeated with similar results. (c) In vitro antibody secretion. Supernatants from resting B cells stimulated for 4 days with LPS were assayed for total IgM and IgG by sandwich ELISA. Error bars show s.e.m. from 4 mice per group. *P <0.05 Experiment was repeated with similar results. (d) In vivo plasma cell formation. Slc3a2f/fCD19-Cre+ and control mice were immunized with TNP-KLH in CFA. One wk later, splenocytes were cultured for 2–3 h on TNP-coated PVDF membrane 96-well plates. After washing to remove cells, and incubation with anti-IgG HRP-conjugated secondary antibody, AEC substrate was used to develop red spots indicating TNP-specific IgG-secreting plasma cells. Error bars indicate s.e.m. from 4 mice for each group (*P = 0.05, **P = 0.08). Experiment was repeated once.