Immunoregulation by tumor necrosis factor superfamily member LIGHT

Yugang Wang, Mingzhao Zhu, Mendy Miller, Yang Xin Fu

Research output: Contribution to journalReview articlepeer-review

30 Scopus citations


LIGHT (homologous to lymphotoxins, inducible expression, competes with herpesvirus glycoprotein D for herpesvirus entry mediator, a receptor expressed on T lymphocytes) is a member of the tumor necrosis factor superfamily that contributes to the regulation of immune responses. LIGHT can influence T-cell activation both directly and indirectly by engagement of various receptors that are expressed on T cells and on other types of cells. LIGHT, LIGHT receptors, and their related binding partners constitute a complicated molecular network in the regulation of various processes. The molecular cross-talk among LIGHT and its related molecules presents challenges and opportunities for us to study and to understand the full extent of the LIGHT function. Previous research from genetic and functional studies has demonstrated that dysregulation of LIGHT expression can result in the disturbance of T-cell homeostasis and activation, changing the ability of self-tolerance and of the control of infection. Meanwhile, blockade of LIGHT activity can ameliorate the severity of various T-cell-mediated diseases. These observations indicate the importance of LIGHT and its involvement in many physiological and pathological conditions. Understanding LIGHT interactions offers promising new therapeutic strategies that target LIGHT-engaged pathways to fight against cancer and various infectious diseases.

Original languageEnglish (US)
Pages (from-to)232-243
Number of pages12
JournalImmunological Reviews
Issue number1
StatePublished - May 2009


  • Autoimmune disease
  • Cytokines
  • T cells
  • TNF superfamily

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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