IL-23p19 缺陷型 BALB/c 小鼠中 Th17 细胞生成不足可防止进行性皮肤利什曼病。
Insufficient generation of Th17 cells in IL-23p19-deficient BALB/c mice protects against progressive cutaneous leishmaniasis.
机构信息
Department of Dermatology, University Hospital of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Institute of Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
出版信息
Exp Dermatol. 2018 Jan;27(1):101-103. doi: 10.1111/exd.13455. Epub 2017 Dec 6.
Healing of leishmaniasis-a parasitic skin disease-is associated with high levels of secreted interferon (IFN)γ and IL-12 in resistant C57BL/6 mice and humans. Susceptible BALB/c mice predominantly react with a Th17/Th2/Treg-related immune response and finally succumb to infection. Previously, we showed that BALB/c IL-17A mice are protected against Leishmania (L.) major infections, indicating that IL-17A-predominantly produced by Th17 cells-plays an important role for disease outcome. We now investigated DC-derived cytokines and finally identified IL-23p19 as key cytokine responsible for induction of Leishmania-specific Th17 cells that play an important role for progressive disease in susceptible BALB/c mice.
利什曼病（一种寄生虫性皮肤疾病）的治愈与抵抗性 C57BL/6 小鼠和人类中高水平的分泌型干扰素（IFN）γ和 IL-12 有关。易感性 BALB/c 小鼠主要表现出 Th17/Th2/Treg 相关免疫反应，最终会感染。先前，我们表明 BALB/c IL-17A 小鼠可免受利什曼原虫（L.）主要感染的影响，表明主要由 Th17 细胞产生的 IL-17A 在疾病结局中起着重要作用。现在，我们研究了 DC 衍生的细胞因子，最终确定 IL-23p19 是诱导利什曼原虫特异性 Th17 细胞的关键细胞因子，这些细胞在易感 BALB/c 小鼠的进行性疾病中起着重要作用。
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