AI Article Synopsis
- Lymphotoxin LTalpha(1)beta(2) is essential for the development and maintenance of spleen structure, particularly in organizing marginal sinus (MS) vessels.
- In lymphotoxin-deficient mice, early white pulp vessels failed to organize properly, affecting both endothelial and smooth muscle cells.
- LTalpha(1)beta(2) plays a crucial role in maintaining MAdCAM-1 expression and the mature MS structure, which is important for immune cell movement in response to bacterial infections.
Article Abstract
The lymphotoxin LTalpha(1)beta(2) supports the development and maintenance of several aspects of spleen structure, but its significance for marginal sinus (MS) vascular organization is unclear. We showed here that, in early postnatal lymphotoxin-deficient mice, the developing Flk-1+ white pulp vessels failed to organize or upregulate MAdCAM-1, leading to altered spatial rearrangement of both the white pulp endothelial cells and the smooth muscle actin-expressing cells. In vitro, MAdCAM-1 directed the reorganization of LTbeta receptor+ endothelial cells grown on Matrigel. LTalpha(1)beta(2) also regulated the maintenance of both MAdCAM-1 expression and mature MS structure in adult mice, contributing importantly to normal trafficking of CD11b+ cells in response to bacterial antigens. Together, our studies demonstrate that LTalpha(1)beta(2) and LTbeta receptor signals control proper development and maintenance of the mature MS structure and implicate MAdCAM-1 in the structuring of the MS endothelial cells that is important for the movement of immune cells within the spleen.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874947 | PMC |
| http://dx.doi.org/10.1016/j.immuni.2009.01.010 | DOI Listing |
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