| First Author | Dubey LK | Year | 2016 |
| Journal | Cell Rep | Volume | 15 |
| Issue | 7 | Pages | 1527-1541 |
| PubMed ID | 27160906 | Mgi Jnum | J:235461 |
| Mgi Id | MGI:5796432 | Doi | 10.1016/j.celrep.2016.04.023 |
| Citation | Dubey LK, et al. (2016) Lymphotoxin-Dependent B Cell-FRC Crosstalk Promotes De Novo Follicle Formation and Antibody Production following Intestinal Helminth Infection. Cell Rep 15(7):1527-41 |
| abstractText | Secondary lymphoid tissues provide specialized niches for the initiation of adaptive immune responses and undergo a remarkable expansion in response to inflammatory stimuli. Although the formation of B cell follicles was previously thought to be restricted to the postnatal period, we observed that the draining mesenteric lymph nodes (mLN) of helminth-infected mice form an extensive number of new, centrally located, B cell follicles in response to IL-4Ralpha-dependent inflammation. IL-4Ralpha signaling promoted LTalpha1beta2 (lymphotoxin) expression by B cells, which then interacted with CCL19 positive stromal cells to promote lymphoid enlargement and the formation of germinal center containing B cell follicles. Importantly, de novo follicle formation functioned to promote both total and parasite-specific antibody production. These data reveal a role for type 2 inflammation in promoting stromal cell remodeling and de novo follicle formation by promoting B cell-stromal cell crosstalk. |
