Immunoregulation by tumor necrosis factor superfamily member LIGHT

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

Research output: Contribution to journalReview article

22 Citations (Scopus)

Abstract

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
Volume229
Issue number1
DOIs
StatePublished - May 1 2009

Fingerprint

Tumor Necrosis Factor-alpha
Light
T-Lymphocytes
Receptors, Tumor Necrosis Factor, Member 14
Self Tolerance
Lymphotoxin-alpha
Genetic Research
Herpesviridae
Communicable Diseases
Glycoproteins
Homeostasis
Infection

Keywords

  • Autoimmune disease
  • Cytokines
  • T cells
  • TNF superfamily

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Immunoregulation by tumor necrosis factor superfamily member LIGHT. / Wang, Yugang; Zhu, Mingzhao; Miller, Mendy; Fu, Yang Xin.

In: Immunological Reviews, Vol. 229, No. 1, 01.05.2009, p. 232-243.

Research output: Contribution to journalReview article

Wang, Yugang ; Zhu, Mingzhao ; Miller, Mendy ; Fu, Yang Xin. / Immunoregulation by tumor necrosis factor superfamily member LIGHT. In: Immunological Reviews. 2009 ; Vol. 229, No. 1. pp. 232-243.
@article{707ef874bf654dda88a58a68023fffc5,
title = "Immunoregulation by tumor necrosis factor superfamily member LIGHT",
abstract = "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.",
keywords = "Autoimmune disease, Cytokines, T cells, TNF superfamily",
author = "Yugang Wang and Mingzhao Zhu and Mendy Miller and Fu, {Yang Xin}",
year = "2009",
month = "5",
day = "1",
doi = "10.1111/j.1600-065X.2009.00762.x",
language = "English (US)",
volume = "229",
pages = "232--243",
journal = "Immunological Reviews",
issn = "0105-2896",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Immunoregulation by tumor necrosis factor superfamily member LIGHT

AU - Wang, Yugang

AU - Zhu, Mingzhao

AU - Miller, Mendy

AU - Fu, Yang Xin

PY - 2009/5/1

Y1 - 2009/5/1

N2 - 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.

AB - 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.

KW - Autoimmune disease

KW - Cytokines

KW - T cells

KW - TNF superfamily

UR - http://www.scopus.com/inward/record.url?scp=65349113104&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=65349113104&partnerID=8YFLogxK

U2 - 10.1111/j.1600-065X.2009.00762.x

DO - 10.1111/j.1600-065X.2009.00762.x

M3 - Review article

C2 - 19426225

AN - SCOPUS:65349113104

VL - 229

SP - 232

EP - 243

JO - Immunological Reviews

JF - Immunological Reviews

SN - 0105-2896

IS - 1

ER -