biostudies-literatureUnknown10(4)Zhang G<h4>Background</h4>Cervical cancer is mainly caused by persistent infection with human papillomavirus (HPV), especially HPV-16. Recently, HPV-16 E7-modified dendritic cells (DCs) have been reported to play a blocking role in the progression of cervical cancer. Conversely, the effect and mechanism of HPV-16 E7-pulsed DCs in cervical cancer are not entirely clear.<h4>Methods</h4>DCs from the peripheral blood of patients with cervical cancer were induced with lipopolysaccharide and identified through the detection of cluster of differentiation (CD)11c, major histocompatibility complex (MHC)-II, CD83, and CD40 levels, and exosomes from HPV-16 E7-pulsed and catalase 2 (CAT2)-silenced DCs were extracted and identified through transmission electron microscopy and the detection of markers. Additionally, the migration, inflammatory factors, and polarization of macrophages were confirmed using Transwell, enzyme-linked immunoassay, and Western blot of arginase-1 (Arg-1) and inducible nitric oxide synthase (iNOS). <i>In vivo</i>, we also built a mice xenograft model of HPV cervical cancer.<h4>Results</h4>We first successfully induced and identified DCs from cervical cancer patients, and successfully extracted and confirmed the exosomes from the constructed HPV-16 E7-pulsed and CAT2-silenced DCs. Subsequently, we proved that exosomes from HPV-16 E7-pulsed DCs restrained migration and inflammation and induced M2 polarization in macrophages, while the effect of exosomes from CAT2-silenced DCs on macrophage migration, polarization, and inflammation was opposite to that of exosomes from HPV-16 E7-pulsed DCs, and the 2 affected each other. Additionally, we found that exosomes from CAT2-silenced DCs also prevented growth and M2 polarization in a mice xenograft model of HPV cervical cancer.<h4>Conclusions</h4>Exosomes from HPV-16 E7-pulsed DCs blocked cervical cancer progression by regulating macrophage function, and its mechanism was relevant to CAT2.Annals of translational medicine217https://www.ebi.ac.uk/biostudies/studies/S-EPMC8908111biostudies-literatureExosomes from HPV-16 E7-pulsed dendritic cells prevent the migration, M1 polarization, and inflammation of macrophages in cervical cancer by regulating catalase 2 (CAT2).PMC8908111Zhang GPan XLiao YZhang XfalseExosomes from HPV-16 E7-pulsed dendritic cells prevent the migration, M1 polarization, and inflammation of macrophages in cervical cancer by regulating catalase 2 (CAT2).<h4>Background</h4>Cervical cancer is mainly caused by persistent infection with human papillomavirus (HPV), especially HPV-16. Recently, HPV-16 E7-modified dendritic cells (DCs) have been reported to play a blocking role in the progression of cervical cancer. Conversely, the effect and mechanism of HPV-16 E7-pulsed DCs in cervical cancer are not entirely clear.<h4>Methods</h4>DCs from the peripheral blood of patients with cervical cancer were induced with lipopolysaccharide and identified through the detection of cluster of differentiation (CD)11c, major histocompatibility complex (MHC)-II, CD83, and CD40 levels, and exosomes from HPV-16 E7-pulsed and catalase 2 (CAT2)-silenced DCs were extracted and identified through transmission electron microscopy and the detection of markers. Additionally, the migration, inflammatory factors, and polarization of macrophages were confirmed using Transwell, enzyme-linked immunoassay, and Western blot of arginase-1 (Arg-1) and inducible nitric oxide synthase (iNOS). <i>In vivo</i>, we also built a mice xenograft model of HPV cervical cancer.<h4>Results</h4>We first successfully induced and identified DCs from cervical cancer patients, and successfully extracted and confirmed the exosomes from the constructed HPV-16 E7-pulsed and CAT2-silenced DCs. Subsequently, we proved that exosomes from HPV-16 E7-pulsed DCs restrained migration and inflammation and induced M2 polarization in macrophages, while the effect of exosomes from CAT2-silenced DCs on macrophage migration, polarization, and inflammation was opposite to that of exosomes from HPV-16 E7-pulsed DCs, and the 2 affected each other. Additionally, we found that exosomes from CAT2-silenced DCs also prevented growth and M2 polarization in a mice xenograft model of HPV cervical cancer.<h4>Conclusions</h4>Exosomes from HPV-16 E7-pulsed DCs blocked cervical cancer progression by regulating macrophage function, and its mechanism was relevant to CAT2.2022-01-01T00:00:00Z2022 Feb2025-04-04T10:44:51.139Z2024-11-21T05:30:33.007ZS-EPMC89081113528039010.21037/atm-21-6998