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Different role of IL-4 in the onset of hapten-induced contact hypersensitivity in BALB/c and C57BL/6 mice

机译:IL-4在BALB / c和C57BL / 6小鼠半抗原诱发的超敏反应发作中的不同作用

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摘要

class="enumerated" style="list-style-type:decimal">To study the role of interleukin (IL)-4 in the onset of contact hypersensitivity (CH) in mice, the effect of IL-4 gene-depletion and anti-IL-4 monoclonal antibody treatment on dinitrofluorobenzene (DNFB)-induced CH was examined. Simultaneously, to clarify the effect of background gene, DNFB-induced CH in BALB/c and C57BL/6 mice was compared.Five repeated topical applications of DNFB to the ears of mice resulted in CH of the ears in terms of increases in ear thickness and histopathological changes. The magnitude of ear thickness increase in BALB/c mice was almost three times greater than that in C57BL/6 mice.The CH in BALB/c mice was significantly suppressed by IL-4 gene-depletion and anti-IL-4 monoclonal antibody treatment. In contrast, the symptoms of dermatitis in C57BL/6 mice were slightly affected by the same treatment. These changes corresponded well to the production of specific IgE antibody.Total IgE antibody production and the expression of productive Cε mRNA were dramatically suppressed by IL-4 gene-depletion and anti-IL-4 treatment in BALB/c and C57BL/6 mice. Neither total IgG nor IgM levels in either strain of mice was altered by depletion of IL-4.The expression of IFN-γ in the skin lesion was dramatically suppressed by IL-4 gene-depletion in BALB/c mice, but not in C57BL/6 mice.These findings indicate that IL-4 plays an important role in the onset of DNFB-induced CH in BALB/c mice, but not in C57BL/6 mice.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 为了研究白介素(IL)-4在小鼠接触性超敏反应(CH)发作中的作用,研究了IL-4基因缺失和抗IL-4单克隆抗体治疗对二硝基氟苯(DNFB)诱导的CH的作用。检查。同时,为了阐明背景基因的作用,比较了DNFB诱导的BALB / c和C57BL / 6小鼠的CH的发生。 对小鼠的耳朵反复局部应用DNFB五次,导致了耳的CH耳朵厚度增加和组织病理学改变方面。 BALB / c小鼠的耳厚增加幅度几乎是C57BL / 6小鼠的三倍。 IL-4基因缺失和抗血清可显着抑制BALB / c小鼠的CH -IL-4单克隆抗体治疗。相反,C57BL / 6小鼠的皮肤炎症状受到相同治疗的影响。这些变化与特异性IgE抗体的产生非常吻合。 IL-4基因缺失和抗IL-4处理可显着抑制总IgE抗体产生和生产性CεmRNA的表达。 c和C57BL / 6小鼠。 IL-4的耗竭不会改变任何小鼠品系中的总IgG和IgM水平。 IL-4基因耗竭可显着抑制BALB /小鼠皮肤病变中IFN-γ的表达。 c小鼠,但不是C57BL / 6小鼠。 这些发现表明,IL-4在DNFB诱导的BALB / c小鼠CH发病中起重要作用,而在C57BL / 6小鼠中则没有

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