Inflammasome activation of IL-1 family mediators in response to cutaneous photodamage.
Inflammasome activation of IL-1 family mediators in response to cutaneous photodamage.
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DOI：
10.1111/j.1751-1097.2012.01182.x
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发表时间：
2012-09
影响因子：
3.3
通讯作者：
Timares L
中科院分区：
文献类型：
--
作者：
Nasti TH;Timares L
尽管角质形成细胞对紫外线辐射 (UVR) 引起的损伤相对有抵抗力，但反复暴露于 UVR 会导致累积的 DNA 突变，从而导致表皮恶性肿瘤。角质形成细胞在导致炎症并影响皮肤适应性免疫反应生成的先天反应中发挥着核心作用。除了表皮的次要细胞成分，特别是朗格汉斯细胞和黑素细胞外，角质形成细胞是细胞因子的主要来源。 UVR 暴露刺激角质形成细胞分泌丰富的促炎性 IL-1 家族蛋白、IL-1α、IL-1β、IL-18 和 IL-33。正常皮肤仅含有低水平的无活性前体形式的 IL-1β 和 IL-18，其成熟和分泌需要 caspase 1 介导的蛋白水解作用。然而，caspase-1 的激活不是组成型的，而是依赖于紫外线诱导的活性炎症体复合物的形成。 IL-1 家族细胞因子可诱导来自角质形成细胞和其他细胞的介质和细胞因子的二次级联，导致广泛的先天过程，包括炎性白细胞浸润、诱导免疫抑制、DNA 修复或细胞凋亡。因此，角质形成细胞产生多种促炎细胞因子的能力可以影响局部和系统的免疫反应，并改变宿主对光损伤细胞的反应。我们将强调由紫外线损伤的角质形成细胞产生的每个 IL-1 家族分子所发挥的不同作用，并揭示它们在调节皮肤紫外线暴露后的急性炎症和免疫事件中的互补影响。
Although keratinocytes are relatively resistant to ultraviolet radiation (UVR) induced damage, repeated UVR exposure result in accumulated DNA mutations that can lead to epidermal malignancies. Keratinocytes play a central role in elaborating innate responses that lead to inflammation and influence the generation of adaptive immune responses in skin. Apart from the minor cellular constituents of the epidermis, specifically Langerhans cells and melanocytes, keratinocytes are the major source of cytokines. UVR exposure stimulates keratinocytes to secrete abundant pro-inflammatory IL-1-family proteins, IL-1α, IL-1β, IL-18 and IL-33. Normal skin contains only low levels of inactive precursor forms of IL-1β and IL-18, which require caspase 1-mediated proteolysis for their maturation and secretion. However, caspase-1 activation is not constitutive, but dependents on the UV-induced formation of an active inflammasome complex. IL-1 family cytokines can induce a secondary cascade of mediators and cytokines from keratinocytes and other cells resulting in wide range of innate processes including infiltration of inflammatory leukocytes, induction of immunosuppression, DNA repair or apoptosis. Thus, the ability of keratinocytes to produce a wide repertoire of proinflammatory cytokines can influence the immune response locally as well as systematically, and alter the host response to photodamaged cells. We will highlight differential roles played by each IL-1 family molecule generated by UV-damaged keratinocytes, and reveal their complementary influences in modulating acute inflammatory and immunological events that follow cutaneous UV exposure.
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DOI：
10.1073/pnas.0812690106
发表时间：
2009-06-02
影响因子：
11.1
作者：
Cayrol, Corinne;Girard, Jean-Philippe
通讯作者：
Girard, Jean-Philippe
影响因子：
16
作者：
Afonina IS;Tynan GA;Logue SE;Cullen SP;Bots M;Lüthi AU;Reeves EP;McElvaney NG;Medema JP;Lavelle EC;Martin SJ
通讯作者：
Martin SJ
影响因子：
17.1
作者：
Dawes JM;Calvo M;Perkins JR;Paterson KJ;Kiesewetter H;Hobbs C;Kaan TK;Orengo C;Bennett DL;McMahon SB
通讯作者：
McMahon SB
DOI：
10.1073/pnas.0611496104
发表时间：
2007-05-08
影响因子：
11.1
作者：
Duncan, Joseph A.;Bergstralht, Daniel T.;Ting, Jenny Pan-Yun
通讯作者：
Ting, Jenny Pan-Yun
影响因子：
15.9
作者：
Coughlin, CM;Salhany, KE;Lee, WMF
通讯作者：
Lee, WMF