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2009 ; 229
(1
): 232-43
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gab.com Text
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English Wikipedia
Immunoregulation by tumor necrosis factor superfamily member LIGHT
#MMPMID19426225
Wang Y
; Zhu M
; Miller M
; Fu YX
Immunol Rev
2009[May]; 229
(1
): 232-43
PMID19426225
show ga
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.
|Animals
[MESH]
|Atherosclerosis/immunology/metabolism
[MESH]
|Dendritic Cells/*immunology/metabolism
[MESH]
|Graft vs Host Disease/immunology/metabolism
[MESH]