Both the lymphotoxin and tumor necrosis factor pathways are involved in experimental murine models of colitis

Dysregulated LIGHT expression on T cells mediates intestinal inflammation and contributes to IgA nephropathy

“…Administration of LTβR-Ig, a soluble receptor for LIGHT, significantly reduced the accumulation of glomerular IgA in LP/J recipients, suggesting involvement of LIGHT and disturbance of the LTβR pathway as a common mechanism for the pathogenesis IgAN. Previous studies have shown that treatment with LTβR-Ig can block the development of GVHD (20) and colitis (41) and that GALT is the major site initiating the GVHD responses (42). Therefore, an alternative explanation for the effects of LTβR-Ig on IgAN may be reduced GVHD or colitis mediated by LTβR-IG treatment, and specific involvement of gut IgA production needs to be further elucidated.…”

Role of Janus Kinase 3 in Mucosal Differentiation and Predisposition to Colitis

“…Tissue cross-sections (5-10 m thick) were stained with hematoxylin and eosin (H&E) using standard protocol. The mean degree of acute colitis in the colon was calculated from observation of 25 different fields of H&E-stained sections of colon from each animal (20). The degree of colitis was evaluated by the following histopathological score grading system.…”

LIGHT Is Constitutively Expressed on T and NK Cells in the Human Gut and Can Be Induced by CD2-Mediated Signaling

“…TNF is implicated as an important contributor to intestinal inflammation with a subset of patients with CD responding to anti-TNF therapy (9). However, the partial success of blocking TNF emphasizes the complexity of mucosal immune regulatory mechanisms, prompting an investigation of other TNF-related ligands, such as lymphotoxin (LT) ␣␤ and lymphotoxin-like inducible protein that competes with glycoprotein D for binding herpesvirus entry mediator on T cells (LIGHT), in human IBD pathology (2,10,11).…”