Figure 2.
Figure 2. CXCL13 induces B-cell adhesion to ICAM-1 and MAdCAM-1 under static conditions. B cells were stimulated with CXCL13 and allowed to bind to immobilized ICAM-1 (A,C,E), MAdCAM-1 (B,D,F), or control IgG. PMA was used as a positive control. After the unbound B cells were washed off, the bound B cells were counted. The binding of B cells to ICAM-1 (A) was abrogated by mAbs to ICAM-1 or CD11a (C) or by PTX (E). Similarly, the CXCL13-induced B-cell binding to MAdCAM-1 (B) was inhibited by mAbs to CD49d or MAdCAM-1 (D) or by PTX (F). Data represent the mean ± SD of the number of bound B cells in triplicate fields. *P < .05 compared with untreated B cells. **P < .01 compared with untreated B cells. ***P < .01 compared with control IgG- or vehicle-treated B cells.

CXCL13 induces B-cell adhesion to ICAM-1 and MAdCAM-1 under static conditions. B cells were stimulated with CXCL13 and allowed to bind to immobilized ICAM-1 (A,C,E), MAdCAM-1 (B,D,F), or control IgG. PMA was used as a positive control. After the unbound B cells were washed off, the bound B cells were counted. The binding of B cells to ICAM-1 (A) was abrogated by mAbs to ICAM-1 or CD11a (C) or by PTX (E). Similarly, the CXCL13-induced B-cell binding to MAdCAM-1 (B) was inhibited by mAbs to CD49d or MAdCAM-1 (D) or by PTX (F). Data represent the mean ± SD of the number of bound B cells in triplicate fields. *P < .05 compared with untreated B cells. **P < .01 compared with untreated B cells. ***P < .01 compared with control IgG- or vehicle-treated B cells.

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