Immunoregulation by tumor necrosis factor superfamily member LIGHT.
Immunoregulation by tumor necrosis factor superfamily member LIGHT.
复制标题
肿瘤坏死因子超家族成员光的免疫调节。
DOI：
10.1111/j.1600-065x.2009.00762.x
复制
发表时间：
2009-05
影响因子：
8.7
通讯作者：
Fu YX
中科院分区：
文献类型：
--
作者：
Wang Y;Zhu M;Miller M;Fu YX
LIGHT（与淋巴毒素同源，可诱导表达，与疱疹病毒糖蛋白D竞争疱疹病毒进入介质，一种在T淋巴细胞上表达的受体）是肿瘤坏死因子超家族的成员，有助于调节免疫反应。光可以通过参与在T细胞和其他类型细胞上表达的各种受体，直接或间接地影响T细胞的激活。光、光受体及其相关结合伙伴构成了一个复杂的分子网络，对各种过程进行调控。光及其相关分子之间的分子串扰为我们研究和全面了解光的功能提供了挑战和机遇。先前的遗传和功能研究表明，LIGHT表达失调可导致t细胞稳态和激活紊乱，改变自身耐受和控制感染的能力。同时，阻断LIGHT活性可以改善各种t细胞介导的疾病的严重程度。这些观察结果表明LIGHT及其参与许多生理和病理条件的重要性。了解光相互作用提供了有希望的新治疗策略，针对光参与途径对抗癌症和各种传染病。
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.