Abstract
This review focuses on the role of homologous to lymphotoxin, exhibits inducible expression, competes with herpesvirus glycoprotein D for HVEM on T cells (LIGHT) in T-cell immunity and T cell-mediated diseases. LIGHT binds to lymphotoxin-β receptor (LTβR), and cooperates with LTβ in lymphoid organogenesis and development of lymphoid structure. Previous findings establish a crucial biological role for LIGHT, a T cell-derived costimulatory ligand, in T-cell activation and expansion via a T-T cell-dependent manner. Transgenic studies demonstrated that the dysregulation of LIGHT activity results in the disturbance of T-cell homeostasis and ultimately the breakdown of peripheral tolerance. Furthermore, the blockade of LIGHT activity ameliorates the severity of T cell-mediated diseases indicating the essential involvement of LIGHT in various pathological conditions. Here, we review the recent studies about LIGHT mainly in the context of autoimmunity and conclude with a discussion of the potential mechanisms by which LIGHT promotes autoimmunity.
Original language | English (US) |
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Pages (from-to) | 201-214 |
Number of pages | 14 |
Journal | Immunologic Research |
Volume | 30 |
Issue number | 2 |
DOIs | |
State | Published - 2004 |
Keywords
- Autoimmunity
- Chemokine
- Costimulation
- HVEM
- LIGHT
- LTβR
- Lymphoid Structure
- T cell-mediated diseases
- T-cell activation
ASJC Scopus subject areas
- Immunology