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of gp38(+)CD31(-) which are PDGFα PDGFβ and Th17 cells was also found to be required to propagate
PDGFα PDGFβ ], which closely resembled lymph inflammation and disease progress in Th17 cell A/T EAE
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node fibroblastic reticular cells, were dramatically model. Moreover, increased levels of Ltαβ (LTBR ligand)
[7]
increased in EAE meninges regardless of the genetic on activated CD4+ T cells were found in MS patients, but
[7]
background of mice. From in vivo and in vitro not in healthy controls. [7]
studies, they found that Th17 cells and their soluble
mediators IL-17 and IL-22 could remodel fibroblasts Collectively, these results suggest that infiltrating
and up-regulate extracellular matix proteins and Th17 cells remodel the meningeal stromal cells
metal matrix proteinase 9, chemokines (murine and initiate the formation of TLTs during EAE.
macrophage inflammatory protein-3α, murine The remodeled stromal cells retain and promote
exodus-2, human GRO/melanoma growth stimulatory the production of Th17 and the accumulation of B
activity), and cytokines in the meninges. Inhibition cells. The collaboration between LTB on Th17 cells
of both IL-17 and IL-22 resulted in reductions in the and LTBR on meningeal radio-resistant cells is very
fibronectin network and clinical severity of disease. crucial for the induction and progression of MS. This
[7]
These results indicate that infiltrating Th17 cells highlights the importance of the interaction between
contribute to building a suitable environment in the immune cells and non-immune cells (stromal cells)
meninges to support their survival. in the pathogenesis of MS.

How do stromal cells in TLTs support infiltrating Financial support and sponsorship
Th17 cell retention and proliferation in the meninges? Nil.
Lymphotoxin beta receptor (LTBR) is a member of the
tumor necrosis factor superfamily and is expressed on Conflicts of interest
[8]
stromal cells, dendritic cells, and macrophages, whereas There are no conflicts of interest.
its ligand LTab is expressed on embryonic Lymphoid
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146 Neuroimmunol Neuroinflammation | Volume 3 | June 20, 2016