Isbell Madison, Mirshahi Faridoddin, Aqbi Hussein F, Guo Chunqing, Saneshaw Mulugeta, Koelsch Nicholas, Idowu Michael O, Austin Dana, Gelber Cohava, Wang Xiang-Yang, Sanyal Arun J, Manjili Masoud H
Department of Microbiology & Immunology, VCU School of Medicine, Richmond, VA 23298, USA.
VCU Massey Cancer Center, 401 College Street, Richmond, VA 23298, USA.
Cancers (Basel). 2022 Nov 9;14(22):5502. doi: 10.3390/cancers14225502.
Predominant inflammatory immunological patterns as well as the depletion of CD4 T cells during nonalcoholic fatty liver disease (NAFLD) are reported to be associated with the progression of hepatocellular carcinoma (HCC). Here, we report that an LRP-1 agonistic peptide, SP16, when administered during advanced NAFLD progression, restored the depleted CD4 T cell population but did not significantly affect the inflammatory immunological pattern. This data suggests that restoration of CD4 T cells without modulation of the hepatic immunological pattern is not sufficient to prevent HCC. However, SP16 administered early during NAFLD progression modulated the inflammatory profile. Future studies will determine if regulation of the inflammatory immune response by SP16 early in NAFLD progression will prevent HCC.
据报道，非酒精性脂肪性肝病（NAFLD）期间主要的炎症免疫模式以及CD4 T细胞的耗竭与肝细胞癌（HCC）的进展有关。在此，我们报告一种LRP-1激动肽SP16，在NAFLD进展晚期给药时，可恢复耗竭的CD4 T细胞群体，但对炎症免疫模式没有显著影响。该数据表明，在不调节肝脏免疫模式的情况下恢复CD4 T细胞不足以预防HCC。然而，在NAFLD进展早期给予SP16可调节炎症特征。未来的研究将确定在NAFLD进展早期通过SP16调节炎症免疫反应是否能预防HCC。
