Gut · 2026
CD16+ γδ T cells mediate antibody-dependent cellular cytotoxicity and associate with viral control in chronic hepatitis B virus infection.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Schröter Paulina E, Steppich Katja, Fernández Carrera Laura, Song Zheng, Klein Sebastian, Souleiman Roni, Urbanek-Quaing Melanie, Lietzau Ayesha D, Schnieders Ansgar, Freyer Erich, Bremer Birgit, León-Lara Ximena, Almeida Vicente, Gutierrez Jauregui Rodrigo, Von Kaisenberg Constantin, Bruhn Matthias, Meineke Carla, Kalinke Ulrich, Wedemeyer Heiner, Prinz Immo, Ravens Sarina, Carpentier Arnaud, Bartsch Yannic Christoph, Kraft Anke R M, Cornberg Markus
Аннотация
BACKGROUND: Chronic hepatitis B virus (HBV) infection is characterised by immune dysfunction. While conventional T cell responses have been extensively studied, the role of γδ T cells, innate-like cytotoxic lymphocytes enriched in the liver, remains incompletely understood.
OBJECTIVE: To characterise γδ T cell subsets in HBV infection and assess their association with viral control and antibody-dependent cellular cytotoxicity (ADCC).
DESIGN: Peripheral blood from patients with chronic (n=83) and acute (n=16) HBV infection, healthy controls (n=31), and cord-blood donors (n=3) was analysed using multiparameter flow cytometry, single-cell RNA sequencing and in vitro ADCC assays.
RESULTS: A distinct CD16+ γδ T cell subset inversely correlated with hepatitis B core-related antigen (HBcrAg), a surrogate of intrahepatic viral replication. CD16+ γδ T cells displayed a cytotoxic signature, whereas CD16⁻ cells showed inflammatory, non-cytotoxic profiles. On hepatitis B surface antigen-specific antibody stimulation, CD16+ γδ T cells mounted potent ADCC responses, mainly mediated by Vδ2+ cells expressing the activating receptor CD226, while Vδ1+ cells preferentially expressed the inhibitory receptor TIGIT. Cytotoxic CD16+ Vδ2+ γδ T cells were present in both blood and liver. CD16+ γδ T cells were expanded and highly functional in acute HBV but reduced and partially impaired in chronic infection. Neonatal cord-blood-derived γδ T cells lacked CD16 expression and displayed limited ADCC potential.
CONCLUSIONS: CD16+ γδ T cells mediate antibody-dependent antiviral immunity in HBV infection. Their inverse association with HBcrAg links γδ T cell-mediated ADCC to viral control and highlights this pathway as a target for HBV cure strategies.
OBJECTIVE: To characterise γδ T cell subsets in HBV infection and assess their association with viral control and antibody-dependent cellular cytotoxicity (ADCC).
DESIGN: Peripheral blood from patients with chronic (n=83) and acute (n=16) HBV infection, healthy controls (n=31), and cord-blood donors (n=3) was analysed using multiparameter flow cytometry, single-cell RNA sequencing and in vitro ADCC assays.
RESULTS: A distinct CD16+ γδ T cell subset inversely correlated with hepatitis B core-related antigen (HBcrAg), a surrogate of intrahepatic viral replication. CD16+ γδ T cells displayed a cytotoxic signature, whereas CD16⁻ cells showed inflammatory, non-cytotoxic profiles. On hepatitis B surface antigen-specific antibody stimulation, CD16+ γδ T cells mounted potent ADCC responses, mainly mediated by Vδ2+ cells expressing the activating receptor CD226, while Vδ1+ cells preferentially expressed the inhibitory receptor TIGIT. Cytotoxic CD16+ Vδ2+ γδ T cells were present in both blood and liver. CD16+ γδ T cells were expanded and highly functional in acute HBV but reduced and partially impaired in chronic infection. Neonatal cord-blood-derived γδ T cells lacked CD16 expression and displayed limited ADCC potential.
CONCLUSIONS: CD16+ γδ T cells mediate antibody-dependent antiviral immunity in HBV infection. Their inverse association with HBcrAg links γδ T cell-mediated ADCC to viral control and highlights this pathway as a target for HBV cure strategies.