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Licensing Virus-Specific T Cells to Secrete the Neutrophil Attracting Chemokine CXCL-8 during Hepatitis B Virus Infection

T cell functional plasticity helps tailor antiviral immunity during different phases of infections. We tested whether, during different phases of HBV infection, virus-specific T cells can acquire specific proinflammatory functions that could drive granulocyte/mononuclear cell liver infiltration. Mul...

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Detalles Bibliográficos
Autores principales: Gehring, Adam J., Koh, Sarene, Chia, Adeline, Paramasivam, Komathi, Chew, Valerie Suk Peng, Ho, Zi Zong, Lee, Kang Hoe, Maini, Mala K., Madhavan, Krishnakumar, Lim, Seng Gee, Bertoletti, Antonio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158071/
https://www.ncbi.nlm.nih.gov/pubmed/21876747
http://dx.doi.org/10.1371/journal.pone.0023330
Descripción
Sumario:T cell functional plasticity helps tailor antiviral immunity during different phases of infections. We tested whether, during different phases of HBV infection, virus-specific T cells can acquire specific proinflammatory functions that could drive granulocyte/mononuclear cell liver infiltration. Multifunctional analysis of HBV-specific T cells during acute and chronic HBV infection revealed that HBV-specific T cells had the capacity to produce the neutrophil chemokine CXCL-8 but not IL-17. CXCL-8 producing T cells were detectable in the liver of chronic HBV patients with active hepatitis; while in acute HBV patients CXCL-8 production by T cells was temporally limited to the acute phase of disease, concomitant with the peak of liver inflammation. Characterization of the conditions necessary for the development of CXCL-8 producing T cells showed a requirement for IL-7 and IL-15 during T cell expansion. These data show that functional plasticity of virus-specific T cells spontaneously occurs during HBV infection and that an environment rich IL-7 and IL-15 can license T cells with the ability to produce CXCL-8 and potentially influence liver pathology.