Figure 5
Figure 5. IL-1R is required for B-cell accumulation and CXCL12 responses. (A) Il1r1−/− mice were injected with IFA and analyzed for accumulation of bone marrow IgD+ cells. Data are pooled from 3 experiments. (B) Total bone marrow from 3 Il1r1−/− mice was plated in CXCL12 chemotaxis assay. Data are representative of 3 independent experiments. (C) A mixed chimera was made with wild-type and Il1r1−/− bone marrow. After reconstitution, mice were challenged with IFA and pooled bone marrow plated in a CXCL12 chemotaxis assay. The figure shows the fold change in chemotaxis of IFA over naive for both CD45.1 and CD45.2 cells. Data are from a single experiment with 6 control and 5 IFA-treated mice. (D) CD45.2 IL-1R–deficient B splenic B cells were transferred into CD45.1 recipients immediately prior to administration of IFA. Transferred cells were enumerated 12 hours later. Data are pooled from 2 experiments.

IL-1R is required for B-cell accumulation and CXCL12 responses. (A) Il1r1−/− mice were injected with IFA and analyzed for accumulation of bone marrow IgD+ cells. Data are pooled from 3 experiments. (B) Total bone marrow from 3 Il1r1−/− mice was plated in CXCL12 chemotaxis assay. Data are representative of 3 independent experiments. (C) A mixed chimera was made with wild-type and Il1r1−/− bone marrow. After reconstitution, mice were challenged with IFA and pooled bone marrow plated in a CXCL12 chemotaxis assay. The figure shows the fold change in chemotaxis of IFA over naive for both CD45.1 and CD45.2 cells. Data are from a single experiment with 6 control and 5 IFA-treated mice. (D) CD45.2 IL-1R–deficient B splenic B cells were transferred into CD45.1 recipients immediately prior to administration of IFA. Transferred cells were enumerated 12 hours later. Data are pooled from 2 experiments.

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