| First Author | Myers RC | Year | 2013 |
| Journal | Eur J Immunol | Volume | 43 |
| Issue | 2 | Pages | 348-59 |
| PubMed ID | 23112125 | Mgi Jnum | J:192842 |
| Mgi Id | MGI:5466642 | Doi | 10.1002/eji.201242471 |
| Citation | Myers RC, et al. (2013) Lymphotoxin alpha(1) beta(2) expression on B cells is required for follicular dendritic cell activation during the germinal center response. Eur J Immunol 43(2):348-59 |
| abstractText | CD19-deficient mice were used as a model to study follicular dendritic cell (FDC) activation because these mice have normal numbers of FDC-containing primary follicles, but lack the ability to activate FDCs or form GCs. It was hypothesized that CD19 expression is necessary for B-cell activation and upregulation of membrane lymphotoxin (mLT) expression, which promotes FDC activation. Using VCAM-1 and FcgammaRII/III as FDC activation markers, it was determined that the adoptive transfer of CD19(+) wild-type B cells into CD19-deficient hosts rescued GC formation and FDC activation, demonstrating that CD19 expression on B cells is required for FDC activation. In contrast, CD19(+) donor B cells lacking mLT were unable to induce VCAM-1 expression on FDCs, furthermore FcgammaRII/III upregulation was impaired in FDCs stimulated with mLT-deficient B cells. VCAM-1 expression on FDCs, but not FcgammaRII/III, was rescued when CD19-deficient B cells expressing transgenic mLT were cotransferred into recipient mice with CD19(+) , mLT-deficient B cells, suggesting that FDC activation requires the CD19-dependent upregulation of mLT on activated B cells. Collectively, these data demonstrate that activated B cells are responsible for the initiation of FDC activation resulting in a microenvironment supportive of GC development and maintenance. |
