The effect of UVB irradiation on antibody responses during herpes simplex virus type 1 (HSV‐1) infections of mice
The effect of UVB irradiation on antibody responses during herpes simplex virus type 1 (HSV‐1) infections of mice
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UVB 照射对小鼠单纯疱疹病毒 1 型 (HSV-1) 感染期间抗体反应的影响
DOI：
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
M. Norval
中科院分区：
文献类型：
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作者：
A. El;G. Horsburgh;M. Norval
中波紫外线(UVB)照射可抑制细胞免疫，并可能改变细胞因子谱，减少辅助性T细胞(Th1)细胞因子，促进Th2细胞因子。Th1细胞因子促进免疫球蛋白(Ig)G2a、IgG2b和IgG3抗体的产生，Th2细胞因子促进IgG1和IgE抗体的产生。用两种方案研究了亚低温UVB照射对C3H/HEN小鼠感染单纯疱疹病毒(HSV)后抗体亚型的影响。首先，在两次皮下感染HSV之前，对小鼠进行了照射。第二，用灭活的HSV免疫小鼠，然后照射并用HSV攻击表皮，这导致了与未照射的动物相比，临床病变的大小增加。在这两种模型中，单纯疱疹病毒特异性免疫球蛋白滴度不受紫外线照射的影响，但一般来说，受照射的动物表现出与Th1和Th2相关的HSV抗体同型的轻微下降。采用IL-4基因敲除(IL-4-/-)小鼠研究IL-4在UVB诱导的同型转换中的作用。在这里，IL-4-/-和IL-4+/+菌株在感染HSV的原发和继发表皮感染之前被照射，随后测量抗体滴度和病变大小。在突变小鼠和亲本小鼠中，紫外线照射导致病变严重程度增加。在IL-4+/+小鼠中，紫外线照射不影响所测试的任何一个个体的HSV滴度，但对HSV的总免疫球蛋白有抑制作用。这种抑制可能是由于紫外线诱导IL-4的释放，因为在IL-4-/-小鼠中，单纯疱疹病毒免疫球蛋白在紫外线照射下升高。如果紫外线仅通过细胞因子的作用来调节免疫应答，那么Th1细胞因子的下调和Th2细胞因子的上调应该伴随着抗体同型从IgG2a和IgG3向IgG1和IgE的转变。在测试的模型中没有得到这一结果，可能是因为HSV感染促进了如此复杂的先天性和获得性免疫反应阵列，以至于对病毒特异性同型生产的明显影响可能并不明显。
Ultraviolet B (UVB) exposure suppresses cell‐mediated immunity and may alter the cytokine profile, reducing T helper 1 (Th1) cytokines and promoting Th2 cytokines. Th1 cytokines enhance the production of immunoglobulin (Ig) G2a, IgG2b and IgG3 antibodies, while Th2 cytokines enhance the production of IgG1 and IgE antibodies. The effect of suberythemal UVB irradiation on antibody isotypes following infection of C3H/HeN mice with herpes simplex virus (HSV) was investigated using two protocols. First, mice were irradiated prior to two subcutaneous infections with HSV. Second, mice were immunised with inactivated HSV before being irradiated and challenged epidermally with HSV, which led to an increase in the size of the clinical lesions compared with unirradiated animals. In both models, the HSV‐specific IgG titre was not affected by the UVB exposure but, generally, the irradiated animals showed a small reduction in both Th1‐ and Th2‐associated HSV antibody isotypes. IL‐4 knockout (IL‐4‐/‐) mice were used to investigate the role of IL‐4 in UVB‐induced isotype switching. Here IL‐4‐/‐ and IL‐4+/+ strains were irradiated prior to primary and secondary epidermal infections with HSV, followed by measurement of antibody titres and lesion size. In both the mutant and parent mice, UV irradiation led to an increase in lesion severity. In IL‐4+/+ mice, UV exposure did not affect the HSV titre of any of the individual isotypes tested but did suppress the total IgG to HSV. This suppression may be due to UV‐induced IL‐4 release because, in the IL‐4‐/‐ mice, HSV IgG was elevated by the UVB irradiation. If UV modulates the immune response solely via the action of cytokines, then the down‐regulation of Th1 cytokines and upregulation of Th2 cytokines should be accompanied by antibody isotype switching from IgG2a and IgG3 towards IgG1 and IgE. This result was not obtained in the models tested, perhaps because HSV infection promotes such a complex array of innate and acquired immune responses that a clear effect on virus‐specific isotype production may not be apparent.
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影响因子：
4.4
作者：
S. Beissert;J. Hosoi;S. Grabbe;A. Asahina;R. Granstein
通讯作者：
S. Beissert;J. Hosoi;S. Grabbe;A. Asahina;R. Granstein
前列腺素参与小鼠暴露于紫外线辐射引起的免疫改变。
DOI：
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发表时间：
1986
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Chung,HT;Burnham,DK;Robertson,B;Roberts,LK;Daynes,RA
通讯作者：
Daynes,RA
局部紫外线照射对小鼠白色念珠菌、牛分枝杆菌卡介苗和曼氏血吸虫感染的影响。
DOI：
10.1111/1523-1747.ep12611853
发表时间：
1992
期刊：
The Journal of investigative dermatology
影响因子：
--
作者：
Jeevan,A;Evans,R;Brown,EL;Kripke,ML
通讯作者：
Kripke,ML
体内证据表明，紫外线 B 诱导的过敏接触敏感性抑制与 Th1 细胞的功能失活有关。
DOI：
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发表时间：
1994
期刊：
Photodermatology, photoimmunology & photomedicine
影响因子：
--
作者：
Simon,JC;Mosmann,T;Edelbaum,D;Schopf,E;Bergstresser,PR;CruzJr,PD
通讯作者：
CruzJr,PD
高剂量 UV-B 辐射会改变人树突状细胞共刺激活性，但不允许树突状细胞在体外使 T 淋巴细胞耐受同种异体抗原。
影响因子：
20.3
作者：
Young,JW;Baggers,J;Soergel,SA
通讯作者：
Soergel,SA