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

Jing Wang, Robert A. Anders, Qiang Wu, Dacheng Peng, Judy H. Cho, Yonglian Sun, Reda Karaliukas, Hyung Sik Kang, Jerrold R. Turner, Yang Xin Fu

Research output: Contribution to journalArticlepeer-review

91 Scopus citations


Whether and how T cells contribute to the pathogenesis of immunoglobulin A nephropathy (IgAN) has not been well defined. Here, we explore a murine model that spontaneously develops T cell-mediated intestinal inflammation accompanied by pathological features similar to those of human IgAN. Intestinal inflammation mediated by LIGHT, a ligand for lymphotoxin β receptor (LTβR), not only stimulates IgA overproduction in the gut but also results in defective IgA transportation into the gut lumen, causing a dramatic increase in serum polymeric IgA. Engagement of LTβR by LIGHT is essential for both intestinal inflammation and hyperserum IgA syndrome in our LIGHT transgenic model. Impressively, the majority of patients with inflammatory bowel disease showed increased IgA-producing cells in the gut, elevated serum IgA levels, and severe hematuria, a hallmark of IgAN. These observations indicate the critical contributions of dysregulated LIGHT expression and intestinal inflammation to the pathogenesis of IgAN.

Original languageEnglish (US)
Pages (from-to)826-835
Number of pages10
JournalJournal of Clinical Investigation
Issue number6
StatePublished - Mar 2004
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)


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