Cao Jinjing, Alvarez Salinas Gerardo Omar, Schmidtke Gunter, Basler Michael
Division of Immunology, Department of Biology, University of Konstanz, Konstanz, Baden-Württemberg, Germany.
Institute of Cell Biology and Immunology Thurgau (BITg), University of Konstanz, Kreuzlingen, Switzerland.
PLoS One. 2025 May 6;20(5):e0323005. doi: 10.1371/journal.pone.0323005. eCollection 2025.
The ubiquitin-like modifier FAT10 is strongly expressed in dendritic cells (DCs) and upregulated during inflammation. Interleukin (IL)-12 plays a critical role in promoting CD4+ T cell differentiation into Th1 cells and in IFN-γ induction in T cells. Previously, it was shown that FAT10 is required for IFN-γ expression of activated T cells. In this study, we investigated whether FAT10 influences IL-12 expression or IL-12 induced signaling and thereby contributes to the reduced IFN-γ expression. Presence or absence of FAT10 did not alter IL-12 expression in DC2.4 cells and in bone marrow derived DCs. Furthermore, FAT10 had no influence on the differentiation of naïve T helper cells to Th1 cells under Th1 polarizing conditions. Additionally, FAT10 did not alter STAT4 phosphorylation in IL-12 receptor stimulated T cells. Taken together, FAT10 neither influences IL-12 expression in DCs nor affects IL-12 receptor signaling in T cells. Hence, the previously observed influence of FAT10 on IFN-γ secretion is not mediated by IL-12.
类泛素修饰因子FAT10在树突状细胞（DCs）中强烈表达，并在炎症过程中上调。白细胞介素（IL）-12在促进CD4+T细胞分化为Th1细胞以及T细胞中IFN-γ诱导方面发挥关键作用。先前有研究表明，FAT10是活化T细胞表达IFN-γ所必需的。在本研究中，我们调查了FAT10是否影响IL-12的表达或IL-12诱导的信号传导，从而导致IFN-γ表达降低。FAT10的存在与否并未改变DC2.4细胞和骨髓来源DCs中IL-12的表达。此外，在Th1极化条件下，FAT10对初始T辅助细胞向Th1细胞的分化没有影响。另外，FAT10不会改变IL-12受体刺激的T细胞中STAT4的磷酸化。综上所述，FAT10既不影响DCs中IL-12的表达，也不影响T细胞中IL-12受体信号传导。因此，先前观察到的FAT10对IFN-γ分泌的影响不是由IL-12介导的。
