| First Author | Ngo VN | Year | 2001 |
| Journal | J Exp Med | Volume | 194 |
| Issue | 11 | Pages | 1649-60 |
| PubMed ID | 11733579 | Mgi Jnum | J:73100 |
| Mgi Id | MGI:2154572 | Doi | 10.1084/jem.194.11.1649 |
| Citation | Ngo VN, et al. (2001) Splenic T zone development is B cell dependent. J Exp Med 194(11):1649-60 |
| abstractText | The factors regulating growth and patterning of the spleen are poorly defined. We demonstrate here that spleens from B cell-deficient mice have 10-fold reduced expression of the T zone chemokine, CCL21, a threefold reduction in T cell and dendritic cell (DC) numbers, and reduced expression of the T zone stromal marker, gp38. Using cell transfer and receptor blocking approaches, we provide evidence that B cells play a critical role in the early postnatal development of the splenic T zone. This process involves B cell expression of lymphotoxin (LT)alpha1beta2, a cytokine that is required for expression of CCL21 and gp38. Introduction of a B cell specific LTalpha transgene on to the LTalpha-deficient background restored splenic CCL21 and gp38 expression, DC numbers, and T zone size. This work also demonstrates that the role of B cells in T zone development is distinct from the effect of B cells on splenic T cell numbers, which does not require LTalpha1beta2. Therefore, B cells influence spleen T zone development by providing: (a) signals that promote T cell accumulation, and: (b) signals, including LTalpha1beta2, that promote stromal cell development and DC accumulation. Defects in these parameters may contribute to the immune defects associated with B cell deficiency in mice and humans. |
