| First Author | Hwang IY | Year | 2009 |
| Journal | J Exp Med | Volume | 206 |
| Issue | 12 | Pages | 2641-57 |
| PubMed ID | 19917774 | Mgi Jnum | J:155452 |
| Mgi Id | MGI:4414569 | Doi | 10.1084/jem.20091982 |
| Citation | Hwang IY, et al. (2009) TLR4 signaling augments B lymphocyte migration and overcomes the restriction that limits access to germinal center dark zones. J Exp Med 206(12):2641-57 |
| abstractText | B lymphocyte-intrinsic Toll-like receptor (TLR) signals amplify humoral immunity and can exacerbate autoimmune diseases. We identify a new mechanism by which TLR signals may contribute to autoimmunity and chronic inflammation. We show that TLR4 signaling enhances B lymphocyte trafficking into lymph nodes (LNs), induces B lymphocyte clustering and interactions within LN follicles, leads to sustained in vivo B cell proliferation, overcomes the restriction that limits the access of nonantigen-activated B cells to germinal center dark zones, and enhances the generation of memory and plasma cells. Intravital microscopy and in vivo tracking studies of B cells transferred to recipient mice revealed that TLR4-activated, but not nonstimulated, B cells accumulated within the dark zones of preexisting germinal centers even when transferred with antigen-specific B cells. The TLR4-activated cells persist much better than nonstimulated cells, expanding both within the memory and plasma cell compartments. TLR-mediated activation of B cells may help to feed and stabilize the spontaneous and ectopic germinal centers that are so commonly found in autoimmune individuals and that accompany chronic inflammation. |
