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. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: J Immunol. 2013 Jun 21;191(3):1055–1062. doi: 10.4049/jimmunol.1201680

Figure 5. No intrinsic defect in Msr1-deficient B cells.

Figure 5

B cells (7 × 106) isolated from Msr1+/+ and Msr1−/− mice were transferred into separate H-2b/g7 T cell-deficient hosts that had received 105 KRN+ T cells one day prior. Eight days later, the congenically-marked donor B cells were analyzed by flow cytometry. GPI-specific B cells of both genotypes show similar (A) activated CD38GL7+ phenotype and (B) Ki67 expression. In control hosts that did not receive KRN+ CD4+ T cells, too few GPI-specific B cells were recovered for analysis (not shown). The numbers indicate the percentage of cells in each quadrant; results are representative of experiments performed with 3 mice/group.