Schieven G L, Ledbetter J A
Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, Washington 98121.
J Immunother Emphasis Tumor Immunol. 1993 Oct;14(3):221-5. doi: 10.1097/00002371-199310000-00009.
Ultraviolet (UV) irradiation is known to suppress normal lymphocyte function, which allows UV phototherapy for a variety of applications. Although UV radiation is well known to cause DNA damage, recent findings indicate that UV irradiation can activate cellular signal-transduction processes. We have previously found that UV induces tyrosine phosphorylation in lymphocytes in a dose- and wavelength-dependent manner and also induces Ca2+ signals in Jurkat T cells via tyrosine phosphorylation of PLC gamma 1 and associated proteins. In this study, normal human lymphocyte subsets were examined for UV-induced Ca2+ responses. CD4+ and CD8+ T cells gave strong responses, whereas other cells did not. Although B cells did not have substantial Ca2+ signals, the pattern of UV-induced tyrosine phosphorylation was very similar to that observed after surface immunoglobulin cross-linking. We propose that the inhibitory effect of UV on lymphocyte function may be due in part to an active induction of tyrosine phosphorylation and Ca2+ signals by a process that bypasses normal receptor control.
已知紫外线（UV）照射会抑制正常淋巴细胞功能，这使得紫外线光疗可用于多种应用。尽管紫外线辐射众所周知会导致DNA损伤，但最近的研究结果表明，紫外线照射可激活细胞信号转导过程。我们之前发现，紫外线以剂量和波长依赖性方式诱导淋巴细胞中的酪氨酸磷酸化，并且还通过PLCγ1及相关蛋白的酪氨酸磷酸化在Jurkat T细胞中诱导Ca2+信号。在本研究中，检测了正常人淋巴细胞亚群对紫外线诱导的Ca2+反应。CD4+和CD8+ T细胞产生强烈反应，而其他细胞则没有。尽管B细胞没有大量的Ca2+信号，但紫外线诱导的酪氨酸磷酸化模式与表面免疫球蛋白交联后观察到的模式非常相似。我们提出，紫外线对淋巴细胞功能的抑制作用可能部分归因于通过绕过正常受体控制的过程对酪氨酸磷酸化和Ca2+信号的主动诱导。
