Traidl C, Jugert F, Krieg T, Merk H, Hunzelmann N
Department of Dermatology, University of Aachen, Germany.
J Invest Dermatol. 1999 Apr;112(4):476-82. doi: 10.1046/j.1523-1747.1999.00550.x.
The role of interleukin-4 as a regulator of immune responses in the skin is investigated with regard to the outcome of contact hypersensitivity reaction in interleukin-4-deficient BALB/C mice. In previous studies conflicting results were obtained concerning the role of interleukin-4 in contact hypersensitivity reactions supporting either a proinflammatory or rather an inhibitory function of this cytokine. Interleukin-4 deficient BALB/C mice sensitized to 2,4-dinitrochlorobenzene showed after challenge a significant reduction in magnitude and duration of the contact hypersensitivity response in comparison with wild-type mice. This attenuation was accompanied by a significant reduction of edema and cellular infiltrates in the dermis and a lacking induction of IL-10 mRNA expression in skin. Also, adoptive transfer experiments revealed that BALB/C mice failed to exhibit contact hypersensitivity after injection of lymph node cells obtained from sensitized interleukin-4 deficient mice. To examine further the role of the contact allergen used to induce the contact hypersensitivity response, mice were also sensitized and challenged with Oxazolone. Here a similar magnitude and duration of contact hypersensitivity in both the interleukin-4 deficient mice and BALB/C control mice was observed. This indicates that the contact hypersensitivity response to 2,4-dinitrochlorobenzene and Oxazolone may partly evolve on different pathways being dependent and independent of interleukin-4. Our results clearly show that the complete loss of endogenous interleukin-4 expression in BALB/C mice is associated with an impaired manifestation of contact hypersensitivity response to 2,4-dinitrochlorobenzene, implying an important proinflammatory function of this cytokine.
关于白细胞介素-4缺陷型BALB/C小鼠接触性超敏反应的结果，研究了白细胞介素-4作为皮肤免疫反应调节因子的作用。在先前的研究中，关于白细胞介素-4在接触性超敏反应中的作用获得了相互矛盾的结果，支持这种细胞因子具有促炎或抑制功能。与野生型小鼠相比，对2,4-二硝基氯苯致敏的白细胞介素-4缺陷型BALB/C小鼠在激发后接触性超敏反应的强度和持续时间显著降低。这种减弱伴随着真皮中水肿和细胞浸润的显著减少以及皮肤中IL-10 mRNA表达的缺乏诱导。此外，过继转移实验表明，BALB/C小鼠在注射从致敏的白细胞介素-4缺陷型小鼠获得的淋巴结细胞后未能表现出接触性超敏反应。为了进一步研究用于诱导接触性超敏反应的接触性变应原的作用，还用恶唑酮对小鼠进行致敏和激发。在此观察到白细胞介素-4缺陷型小鼠和BALB/C对照小鼠的接触性超敏反应强度和持续时间相似。这表明对2,4-二硝基氯苯和恶唑酮的接触性超敏反应可能部分通过不同途径发生，这些途径依赖或不依赖于白细胞介素-4。我们的结果清楚地表明，BALB/C小鼠内源性白细胞介素-4表达的完全丧失与对2,4-二硝基氯苯接触性超敏反应的受损表现相关，这意味着该细胞因子具有重要的促炎功能。
